soal a part 1.pdf

8/14/2019 Soal A part 1.pdf

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PEMBAHASAN TO1

BATCH 1 2013

dr. Himawan, dr. Cemara, dr. Dini,

dr. Yusuf, dr. Ratna, dr. Anshari


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ILMU PENYAKIT DALAM


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1. Komplikasi Kidney Failure

Pasien , 48 tahun

Sulit BAK

Kaki bengkak

Mual muntah Riwayat kencing batu

Kadar ureum 115, kreatinin 5,8, glukosa 168

Jenis Pemeriksaan Nilai Normal Deskripsi

Blood Urea Nitrogen (BUN) 7-25 mg/dL Urea dihasilkan dari metabolismeprotein, difiltrasi di glomerulus. Jika

GFR urea direabsorbsi , kembali

ke aliran darah

Kreatinin 0,6-1,5 mg/dL Produk pemecahan keatinin fosfat dari

otot rangka

Glukosa sewaktu 65-110 mg/dL


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Uremia Symptoms


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Chronic renal failure

Elevated concentration of urea nitrogen

Bacteria produce urease to disintegrateureahigh-concentration nitrogen

Stimulate gastrointestinal mucous

membrane

Nausea & vomiting


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2. HIV

Laki-laki dewasa mudah merasa lemas. Sulit tidur,

nyeri sendi dan otot selama 5 minggu yang lalu.

Nafsu makan baik tetapi merasa BB .

PF : TB 155 cm dan BB 39 kg (IMT = 16,2Underweight). Luka-luka kecil yang menggaung

yang pada awalnya terlihat seperti jerawat.

Lab : CD4 575


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Pathogenesis of HIV

Infection


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How HIV

Infection

Become

AIDS


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HIV Time Course

http://www.microbiologybytes.com


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3. Ikterik

, 40 tahun

Kuning seluruh tubuh sejak 2 minggu yll

BAB dempul

Bilirubin direk , bilirubin indirek normal

Bilirubin direk = conjugated bilirubin

Bilirubin indirek = unconjugated bilirubin


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Type of Jaundice

Wikipedia


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Color Atlas of Pathophysiology


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Color Atlas of Pathophysiology


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Table of Diagnostic Test

Wikipedia


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4. Serologi Hepatitis

, 35 thn

Kuning 4 hari yang lalu, mual, muntah, lemas

Riwayat menggunakan suntik narkotika

PF hepatomegali

SGOT : 100, SGPT : 350, alkali fosfatase 720,

bilirubin total : 8, bilirubin direct 6


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5. Cirrhosis

, 39 tahun

Riwayat peminum alkohol

PF: tampak tidur lelap, kurus, spider nevi (+) di

dinding perut, terdapat bercak darah pada bibirdan bau amandel, ransang nyeri (-)

Lab : ammonia darah meningkat


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Color Atlas of Pathophysiologywww. wikimed.com


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6. Hemostasis

, 61 tahun

Perdarahan sejak 2 jam yll setelah cabut gigi

Penderita jantung koroner dengan konsumsi aspirin

100mg selama beberapa tahun


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Aspirin has anantiplatelet effect by

inhibiting the production

of thromboxane, which

under normalcircumstances

binds plateletmolecules

together to create a

patch over damaged

walls of blood vessels
http://en.wikipedia.org/wiki/Thromboxanehttp://en.wikipedia.org/wiki/Platelethttp://en.wikipedia.org/wiki/Platelethttp://en.wikipedia.org/wiki/Thromboxane


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Hemostasis (hemo=blood; sta=remain) is the

stoppage of bleeding, which is vitally important whenblood vessels are damaged.

Following an injury to blood vessels several actionsmay help prevent blood loss, including:

Formation of a clot


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Formation ofplatelet aggregate

Injured blood vesselreleases ADP, whichattracts platelets (PLT)

PLT comming in contactwith exposed collagenrelease: serotonin, ADP,TXA2, which accelerate

vasoconstriction andcauses PLT to swell andbecome more sticky


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7. Anemia

, 40 tahun

Badan lemas, tidak

nafsu makan, demam(-)

Lab : WBC: 4000gr/dl, Hb: 8 gr/dl, Ht

34% MCV: 114 fl.

Gambaran darah tepi:

netrofil hipersegmen,

makroovalosit


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Anemias are defined based on cell size (MCV) and

amount of Hgb (MCH). MCV lessthan lower limit of normal: microcytic

anemia

MCV within normal range: normocyticanemia

MCV greater than upper limit of normal:macrocytic anemia

MCH less than lower limit of normal:

hypochromic anemia

MCH withinnormal range: normochromicanemia

MCH greater than upper limit of normal:

hyperchromic anemia

Pernicious


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ANEMIA

Impaired RBC production

Disturbance of proliferationand differentiation of stemcells

Disturbance of proliferation

and maturationof erythroblast

Perniciousanemia (megaloblastic

anemia due to vitamin B12deficiency)

Anemia of folic acid

deficiency (megaloblasticanemia)

Anemia of prematurity(premature infants at 2 to 6

weeks of age)

Iron deficiency anemia(deficiency of hemesynthesis)

Thalassemia(deficiencyof globin synthesis)

Congenitaldyserythropoietic anemias

Anemia of renal failure

Increased RBC destruction

(hemolytic anemias)

Intrinsic

Extrinsic

Blood loss

Fluid overload


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MEGALOBLASTIC


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MEGALOBLASTIC

ANEMIA

Anemia (of macrocytic classification)that results from inhibition of DNA

synthesis in red blood cell production

Pathopgenesis

Folate and vitamin B12deficienciesdefective RNA and

DNA syntheses

continuing cell growth without

division

Erythrogenic precursorslarger

than mature red blood cells

(RBCs)

Laboratorium Findings: Decreased red blood cell (RBC) count

and hemoglobin levels[

MCV >95 fl

Increased MCH

Normal MCHC, 3236 g/dL Decreased Reticulocyte count

destruction of fragile and

abnormal megaloblastic erythroid

precursor

Blood smear: hypersegmented neutrophils

macroovalocytes macrocytes with ovalshape RBC

Anisocytosis (increased variation in RBC

size) and poikilocytosis (abnormallyshaped RBCs).

http://emedicine.medscape.com/article/http://en.wikipedia.org/wiki/Megaloblastic_anemia

Gl 6 h h t


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Glucose-6-phosphate

dehydrogenase deficiency

an X-linked recessive hereditary diseasecharacterised by abnormally low levels of glucose-

6-phosphate dehydrogenase

Blood smear: Heinz body in RBC

http://www.diseaseaday.com/wp-

content/uploads/2009/05/g6pddeficiencyprocess.png

http://en.wikipedia.org/wiki/Glucose-6-phosphate_dehydrogenase_deficiency


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8. Kelainan Katup Jantung

, 16 tahun

Sesak napas saat beraktivitas sejak 3 bulan yll

PF: Auskultasi P2 mengeras, opening snap saat diastolik

dengan nada rendah pada apikalis, hepatomegali (-)

Opening Snap

High-frequency early diastolic sound

(occurs 50-100 msec after A2) associatedwith mitral stenosis; sound due to abrupt

deceleration of mitral leaflets sound with

associated murmur


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Loud P2 (pulmonic) component of the(S2)pulmonary hypertension

secondary to severe mitral stenosis

An opening snap heard after the A2

(aortic) component of the (S2)

correlates to the forceful openingof the mitral valve

The mitral valve opens when the

pressure in the left atrium is

greater than the pressure in the

left ventricle

This happens in ventricular

diastole (after closure of the

aortic valve), when the pressure

in the ventricle precipitously

drops


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Pathophysiology of

Mitral Stenosis


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The sounds waves

responsible for heart soundsare generated by vibrations

induced by:

valve closure,

abnormal valve opening, vibrations in the

ventricular chambers,

tensing of the chordae

tendineae, turbulent or abnormal

blood flow across valves

or between cardiac

chambers


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9. Heart Failure

Pasien 59 thn

Sesak napas, riwayat hipertensi dengan BP 150/90

PF : distensi vena leher, krepitasi pada kedua basal

paru, dan edema pada extremitas


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Symptoms of heart failure


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11. Syok Anafilaktik

, 25 thn

Luka robek di kaki akibat kecelakaansuntiklidocaine 1% infiltrasi untuk anestesi luka robeknya

5menit kemudian tjd gatal2 pada ekstremitas,muka flushing, kepala melayang dan sulit bernafas

PF : BP 80/40, HR 84x/menit, RR 32x/menit, suhu

37 c, auskultasi : stridor wheezing


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V dil t ti


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Vasodilatation

mucosaoedema

Oedem

larynx

Stridor


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Brochospasm Wheezing


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12. Acute coronary syndrome

Keluhan 1 jam yang lalu nyeri dada seperti ditindih

beban berat

EKG irama sinus , ST Elevasi V1-V4, denyut jantung

72x/menit, peningkatan enzim jantung serial


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Left coronary artery


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y ymensuplai area: Anterior LV

The bulk of the

interventricular septum(anterior two thirds)

The apex

Lateral and posterior LVwalls

Right coronary arterymensuplai area: Right ventricle (RV)

The posterior third of theinterventricular septum

The inferior wall(diaphragmatic surface) ofthe left ventricle (LV)

A portion of the posteriorwall of the LV (by means ofthe posterior descending

branch)


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EKG


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http://acutemed.co.uk/diseases/ACS+%28Acute+Coronary+Syndrome%29


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13. Spirometri pada PPOK

, 68 tahun

Sesak nafas + batuk sejak 3 minggu, dahak kental

kuning sampai kecoklatan. Riwayat batuk darah

disangkal. Perokok berat sejak usia 17th PF : hemithorax cembung dan perkusi hipersonor di

kedua lapang paru


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Obstructive lung diseasereduced ventilationthe ratio of the

duration of expiration to that of inspiration is increasedobstructedexpiration distends the alveolar ductules (centrilobular emphysema), lung

recoil decreases (compliance increases) and the midposition of breathing

is shifted toward inspiration (barrel chest) raises the functional residual

capacity


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14. Terapi Asma


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p Asma sudah 10 tahun

PF : RR 32x/ menit, FN 110x/ menit

GINA Report 2011


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MANAGEMENTIN STABLE

CONDITION


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Pathophysiology of

Asthma


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http://www.eguidelines.co.uk

Algorithm

of

Asthma

Diagnosis

T i Ok i


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Devices Flow Rate

(L/min

Oxygen

Concentration

Description

Nasal Cannula 15 2844%

Rebreathing

Mask/Simple

Oxygen Mask

6-10 35-60% -First third of exhaled gases mix with

reservoir

-Exhaled gases from upper airwayare oxygen rich

Non Rebreathing

Mask

10-12 95% Two valves added to prevents:

-Entrainment of room air during

inspiration

-Retention of exhaled gases duringexpiration

Venturi Mask 4-8 25-60%

Ventilator can be set 21-100%

Terapi Oksigen


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15 Hi kti it K l j Ad l


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15.Hipoaktivitas Kelenjar Adrenal

, 40 th

Letih lemah sejak 2 bulan yll, saat ini terapi TB,

mengeluh bb turun, dibawah siku warna kulit

tampak menjadi hitam PF : TD 80/50, nadi 72, tidak ada penyakit jantung

Ad l I ffi i


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Adrenal Insufficiency

Adrenal tuberculosis is a manifestation of disseminateddisease presenting rarely as adrenal insufficiency

Addison's disease results from progressive destruction of

the adrenals, which must involve >90% of the glandsbefore adrenal insufficiency appears

The adrenal is a frequent site for chronic granulomatous

diseases, predominantly tuberculosis(70%-90% cases),

but also histoplasmosis, coccidioidomycosis, andcryptococcosis


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Effects and

Symptoms ofAdrenocortical

Hormone

Deficiency


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16. Sindrom CushingCushing's syndrome


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Cushing s syndrome

(hyperadrenocorticalism/hypercortisolism)

The clinical condition resulting from chronic exposure

to excessive circulating levels of glucocorticoids

The most common cause: excess ACTH secretion fromthe anterior pituitary gland (Cushing's disease).

Silbernagl S, et al. Color atlas of pathophysiology. Thieme; 2000.

McPhee SJ, et al. Pathophysiology of disease: an introduction to clinical medicine. 5thed. McGraw-Hill; 2006.


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Acute Effect of Diabetes

Mellitus

(Diabetic Ketoacidosis)

Effect on Insufficiency of Insulin


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Effect on Insufficiency of Insulin

18 Terapi Hipertiroid


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18. Terapi Hipertiroid

, 30 tahun

Dada berdebar-debar sejak 1 minggu yll, gelisah,

sulit tidur, mudah lelah, dan diare

PF : TD 130/80 mmHg, HR 120x/mnt, RR 24x/mnt,mata exopthalmus, pembesara kelenjar tiroid difus,

akral hangat

Laboratorium: peningkatan T3 dan T4, TSH rendah


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Laboratorium Assesment for Thyroid Function


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Laboratorium Assesment for Thyroid Function


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19 Disorder of Calcium Metabolism


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19. Disorder of Calcium Metabolism

, 35 tahun

Pasca tiroidektomi sering mengalami kaku dan

kejang


McPhee SJ, et al. Pathophysiology of disease: an introduction to clinical medicine. 5th

ed. McGraw-Hill 2006.

19. Disorder of


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McPhee SJ, et al. Pathophysiology of disease: an introduction to clinical medicine. 5th

ed. McGraw-Hill; 2006.

Calcium Metabolism

20 Arthritis


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20. Arthritis

Wanita, 30 tahun

Nyeri dan bengkak pada sendi metakarpophalang

dan interfalang kedua tangan, dan bengkak pada

sendi lutut. Dirasakan saat bangun pagi LED 184 mm(), kadar urat serum 6,2 mg/dl

Rheumatoid Arthritis Definition:

Chronic inflammatory

Autoimmune disorder, that affect the joints and may cause systemic

manifestation

Reumatoid Arthritis


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Reumatoid Arthritis

a score of 6 fulfilling the requirements for RA

RA Patophysiology


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RA Patophysiology


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21 Malaria


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21. Malaria

, 25 tahun Penurunan kesadaran 2 jam yll, riwayat demam

hilang timbul, demam tinggi, menggigil dan

keringat dingin PF: TD 100/70 mmHg, S 38,5oC, kulit tampak

pucat, konjungtiva anemis.

Lab : ditemukan plasmodium sausage shape


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Pathogenesis of Cerebral Malaria


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Pathogenesis of Cerebral Malaria

http://www.microbiol.unimelb.edu.au

Possible cause: Binding of

parasitized red cells

in cerebral

capillaries

permeability of the

blood brain barrier

Excessive induction

ofcytokines

22. Dengue Infection


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22. Dengue Infection

, 17 tahun Demam sejak 4 hari yang lalu disertai nyeri kepala,

mual, nyeri otot dan sendi.

PF : TSS, TD 120/80 mmHg, Suhu 38,3C, Nadi98x/menit. Konjungtiva pucat (-). Thoraks: BJ I-IInormal, vesikuler. Abdomen : nyeri tekanepigastrium (+). Ext : petechiae pada lengan ataskanan dan kiri.

Lab: Hb 12 g/dL, hematokrit 36%, Leukosit 4700,Trombosit 98000


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Dengue Infection: Classification


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g


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23 Primary Survey


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23. Primary Survey

A. AirwayEstablish patent airway

B. Breathing

Assess and ensure adequate oxygenation and ventilation

C. Circulation

Level of consciousness Skin color and temperature

Pulse rate and character

D. Disability

Baseline neurologic evaluation

GCS scoringPupillary response

E. Environment

Completely undress the patient

Control hemorrhage Restore volume

Reassess parameters

ATLS


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Secondary Survey


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Secondary Survey

optimized by optima

Componet:

A. History namponade

Allergic Medication Past illness

Last meals EventB. Physical exam : head to toe

C. Every orrifice examination

D. Complete Neurologicalexamination

E. Special diagnostic tests

F. Re-evaluation


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8th ed Schwartz's Principles

of Surgery


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25. ShockDefinition A physiologic state

characterized by Inadequate tissue

perfusion

Clinically manifested by

Hemodynamicdisturbances

Organ dysfunction


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Hypovolemic Shock


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Hypovolemic Shock

Hemorrhagic ShockParameter I II III IV

Blood loss (ml) 2000

Blood loss (%) 40%

Pulse rate(beats/min) 100 >120 >140

Blood pressure Normal Normal Decreased Decreased

Respiratory rate

(bpm) 1420 2030 3040 >35

Urine output

(ml/hour) >30 2030 515 Negligible

CNS symptoms Normal Anxious Confused Lethargic

optimized by optimaCrit Care. 2004; 8(5): 373381.

6. WHO Pain Management Stepladder


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optimized by optima


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Mekanisme kerja opioid


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j p

optimized by optima

27. Hemothorax


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Occurs when pleural space fills with blood Usually occurs due to lacerated blood vessel in

thorax

As blood increases, it puts pressure on heart andother vessels in chest cavity

Each Lung can hold 1.5 liters of blood

Hemothorax27-28 CHEST TRAUMA


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Hemothorax

optimized by optima

Hemothorax


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Hemothorax

Hemothorax


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May put pressure on the heart

Hemothorax

Where does the blood come from.


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Lots of blood vessels

Where does the blood come from.

S/S of Hemothorax


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Anxiety/Restlessness Tachypnea

Signs of Shock

Frothy, Bloody Sputum Diminished Breath Sounds on Affected Side

Tachycardia

Flat Neck Veins

Treatment for Hemothorax


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ABCs with c-spine controlas indicated

Secure Airway assistventilation if necessary

General Shock Care due toBlood loss

Consider Left LateralRecumbent position if notcontraindicated

RAPID TRANSPORT

Contact Hospital and ALSUnit as soon as possible

BLS Plus Care


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Monitor Cardiac Rhythm Establish Large Bore IV preferably 2 and draw

blood samples

Airway management to include Intubation Rapid Transport

If Development of Hemo/Pneumothorax needle

decompression may be indicated

Simple/Closed Pneumothorax


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p /

Opening in lung tissue that

leaks air into chest cavity

Blunt trauma is main cause

May be spontaneous

Usually self correcting


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Open Pneumothorax


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p

Opening in chest cavitythat allows air to enterpleural cavity

Causes the lung to

collapse due toincreased pressure inpleural cavity

Can be life threateningand can deterioraterapidly

Open Pneumothorax


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Inhale


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Exhale

Open Pneumothoraxoptimized by optima

Inhale


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Inhale

Exhale

Open Pneumothorax

Inhale


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Inhale

Exhale

Open Pneumothorax

Open Pneumothorax


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S/S : Dyspnea

Sudden sharp pain

SubcutaneousEmphysema

Decreased lung soundson affected side

Red Bubbles onExhalation from wound(Sucking chest wound)

Th/ :ABCs with c-spine controlas indicatedHigh Flow oxygenListen for decreased

breath sounds on affectedsideApply occlusive dressingto woundNotify Hospital and ALS

unit as soon as possible


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Sucking Chest Wound Occlusive Dressing

28. Tension Pneumothorax


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Air builds in pleuralspace with no where

for the air to escape

Results in collapse of

lung on affected side

that results in pressure

on mediastium,the

other lung, and greatvessels

optimized by optima

Each time we inhale,the lung collapses further.

There is no place for the air to

escape..

Each time we inhale,


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the lung collapses further. There

is no place for the air to

escape..

Heart is being

compressed

The trachea is

pushed to

the good side

S/S of Tension Pneumothorax


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Anxiety/Restlessness Severe Dyspnea

Absent Breath sounds

on affected side Tachypnea

Tachycardia

Poor Color

Accessory Muscle Use JVD

Narrowing Pulse

Pressures Hypotension

Tracheal Deviation

(late if seen at all)

Treatment of Tension Pneumothorax


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ABCs with c-spine as indicated Needle Decompression of Affected Side

High Flow oxygen including BVM

Treat for S/S of Shock Notify Hospital and ALS unit as soon as possible

If Open Pneumothorax and occlusive dressing

present BURP occlusive dressing

Needle Decompression


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Locate 2-3 Intercostal space midclavicular line Cleanse area using aseptic technique

Insert catheter ( 14g or larger) at least 3in length

over the top of the 3rd

rib( nerve, artery, vein liealong bottom of rib)

Remove Stylette and listen for rush of air

Place Flutter valve over catheter

Reassess for Improvement


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29. Ureterolithiasis


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Urinary tract stone disease

Signs: Flank pain

Irritative voiding symptom

Nausea

microscopic hematuria Urinary crystals of calcium

oxalate, uric acid, or cystine

may occasionally be found

upon urinalysis

Diagnosis: IVP

optimized by optima

30. Hirschsprung disease


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Congenital megacolon

the absence of myenteric

and submucosal ganglion

cells in the distal

alimentary tract

decreased motility in theaffected bowel segment

Results from the absence ofparasympathetic ganglion

cells in the myenteric andsubmucosal plexus of therectum and/or colon.

These ganglion cells arrive inthe proximal colon by 8

weeks of gestational ageand in the rectum by 12weeks of gestational age.

Arrest in migration leads toan aganglionic segment.

Definitions Pathophysiology

Hirschsprung disease


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approximately 1 per 5000 livebirths.

Sex: 4 times more common inmales than females.

Age:

Nearly all children withHirschsprung disease arediagnosed during the first 2years of life.

one half are diagnosed beforethey are aged 1 year.

Minority not recognized untillater in childhood or adulthood.

Mortality/Morbidity:

The overall mortality ofHirschsprung enterocolitis is 25-30%,.

Classical HD (75% of cases):Rectosegmoid

Long segment HD (20% ofcases)

Total colonic aganglionosis (3-

12% of cases) rare variants include the

following:

Total intestinal aganglionosis

Ultra-short-segment HD

(involving the distal rectumbelow the pelvic floor and theanus)

Frequency Predilection

Clinical presentation


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Newborns : Failure to pass meconium within

the first 48 hours of life Abdominal distension that is

relieved by rectal stimulation orenemas

Vomiting

Neonatal enterocolitis Symptoms in older children and

adults include the following: Severe constipation Abdominal distension Bilious vomiting

Failure to thrive

Rontgen :

Plain abdominal radiography Dilated bowel

Air-fluid levels.

Empty rectum

Contrast enema Transition zone

Abnormal, irregular contractions ofaganglionic segment

Delayed evacuation of barium

Biopsy : absence of ganglion cells hypertrophy and hyperplasia of

nerve fibers,

HD-Assosciated enterocolitis


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Abdominal distension, explosive diarrhea, vomiting,fever, lethargy, rectal bleeding, or shock

The risk is greatest:

before HD is diagnosed after the definitive pull-through operation.

children with Down syndrome

Treatment


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Surgical removal orbypass of theaganglionic bowel,

Rehydration,

intravenous antibiotics

and colonic irrigations.

Hirschsprung disease HD-Associated enterocolitis

31. Peritonitis


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PeritonitisInfection, or rarely some other type of

inflammation, of the peritoneum.

Peritoneumis a membrane that covers

the surface of both the organs that lie in

the abdominal cavity and the inner

surface of the abdominal cavity itself.

Intra-abdominal infections result in 2 major

clinical manifestations


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Early or diffuse infection results in localized orgeneralized peritonitis.

Late and localized infections produces an intra-abdominal abscess.

2 Major Types


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Primary: Caused by thespread of an infection fromthe blood & lymph nodes tothe peritoneum. Very rare 90 beats/min

Respiratory rate: 29 breaths/min

Urine Output:


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Etiology & Hemodynamic Changes in Shock(Afterload)


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ETIOLOGY OF

SHOCKEXAMPLE CVP CO SVR VO2 SAT

AFTERLOAD DISTRIBUTIVE

Hyperdynamic Septic Low/High High Low High

Hypodynamic Septic Low/High Low High Low/High

Neurogenic Low Low Low Low

Anaphylactic Low Low Low Low

HYPOVOLEMIC SHOCK Decreased preload->small ventricular end-diastolic

volumes > inadequate cardiac generation of pressure and


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volumes -> inadequate cardiac generation of pressure and

flow Causes:

bleeding: trauma, GI bleeding, ruptured aneurysms,hemorrhagic pancreatitis

protracted vomiting or diarrhea

adrenal insufficiency; diabetes insipidus

Dehydration

third spacing: intestinal obstruction, pancreatitis,cirrhosis

Hypovolemic Shock


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Signs & Symptoms: Hypotension, Tachycardia, MS

change, Oliguria, Deminished Pulses.

Markers: monitor UOP,CVP, BP, HR, Hct, MS, CO, lactic

acid and PCWP

Treatment: ABCs, IVF (crystalloid), Trasfusion Stemongoing Blood Loss

SEPTIC/INFLAMMATORY SHOCKMechanism: release of inflammatory mediators leading to


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1. Disruption of the microvascular endothelium2. Cutaneous arteriolar dilation and sequestration of blood in

cutaneous venules and small veins

Causes:

1. Anaphylaxis, drug, toxin reactions

2. Trauma: crush injuries, major fractures, major burns.

3. infection/sepsis: G(-/+ ) speticemia, pneumonia, peritonitis,

meningitis, cholangitis, pyelonephritis, necrotic tissue,pancreatitis, wet gangrene, toxic shock syndrome, etc.


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CARDIOGENIC SHOCKMechanism: Intrinsic abnormality of heart -> inability to


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ec a s t s c ab o a ty o ea t ab ty todeliver blood into the vasculature with adequate power

Causes:

1. Cardiomyopathies: myocardial ischemia, myocardial infarction,cardiomyopathy, myocardiditis, myocardial contusion

2. Mechanical: cardiac valvular insufficiency, papillary muscle rupture,septal defects, aortic stenosis

3. Arrythmias: bradyarrythmias (heart block), tachyarrythmias (atrialfibrillation, atrial flutter, ventricular fibrillation)

4. Obstructive disorders: PE, tension peneumothorax, pericardialtamponade, constrictive pericaditis, severe pulmonary hypertension


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NEUROGENIC SHOCKMechanism: Loss of autonomic


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Causes:

1. Spinal cord injury

2. Regional anesthesia

3. Drugs

4. Neurological disorders

Mechanism: Loss of autonomic

innervation of the cardiovascular system(arterioles, venules, small veins, includingthe heart)

Neurogenic Shock


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Characterized by loss of vascular tone & reflexes. Signs: Hypotension, Bradycardia, Accompanying

Neurological deficits.

Monitor/findings: hemodynamic instability, testbulbo-carvernous reflex

Tx: IVF, vasoactive medications if refractory


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33. FOREHAND FRACTURE

Montegia Fracture Dislocation


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It is a fracture of the proximal

1/3rdof the Ulna with

dislocation of head of radius

anteriorly. Posteriorly or

laterally Head of Radius dislocates

same direction as fracture

It requires ORIF or it willredisplace

Montegia : Lateral displacement


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optimized by optima

Galliazi Fracture


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It is a fracture of distalRadius and dislocation ofinferior Radio- Ulnar joint

Like Montegia fracture iftreated conservatively itwill redisplace

This fracture appeared inacceptable position afterreduction and POP

Greenstick Fractures


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Colles Fracture


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optimized by optima

# distal 1 Impaction ,Dorsal displacementand dorsal tilt


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Colles Fracture


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optimized by optima

Smith Fracture


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Smith Fracture


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Almost the opposite of Colles fracture Much less commoncompared to colles

Results from a fall on palmer flexedwrist

Typical deformity : Garden Spade Management is conservative : MUA and Above

Elbow POP


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34. LOW BACK PAIN

Herniated Nucleus Pulposus


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The progressivedegeneration of a disc, or

traumatic event, can lead

to a failure of the annulus

to adequately contain the

nucleus pulposus

This is known as herniated

nucleus pulposus (HNP) or

a herniated disc



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Symptoms

Back pain

Leg pain

Dysthesias Anesthesias



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Varying degrees Disc bulge

Mild symptoms

Usually go away withnonoperative treatment

Rarely an indicationfor surgery

Extrusion (herniation)

Moderate/severe symptoms

Nonoperative treatment



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Diagnosis

Magnetic resonance imaging(MRI)/patient exam

Nonoperative Care

Initial bed rest

Nonsteroidal anti-inflammatory (NSAID)medication

Physical therapy

Exercise/walking

Steroid injections



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Surgical care

Failure of nonoperativetreatment

Minimum of 6 weeks induration Can be months

Discectomy

Removal of theherniatedportion of the disc

Usually through a smallincision

High success rate



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Cauda Equina Syndrome Caused by a central disc

herniation

Symptoms include bilateral

leg pain, loss of perianal

sensation, paralysis of thebladder, and weakness of

the anal sphincter

Surgical intervention in

these cases is urgent

Spondylolisthesis


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Gradation ofspondylolisthesis

MeyerdingsScale

Grade 1 = up to 25%

Grade 2 = up to 50%

Grade 3 = up to 75%

Grade 4 = up to 100%

Grade 5 >100%

(complete dislocation,

spondyloloptosis)

Spondylolisthesis


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Symptoms

Low back pain

With or without buttock orthigh pain

Pain aggravated by standingor walking

Pain relieved by lying down Concomitant spinal stenosis,

with or without leg pain, maybe present

Other possible symptoms

Tired legs, dysthesias,anesthesias

Partial pain relief by leaningforward or sitting

Spondylolisthesis


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Diagnosis

Plain radiographs

CT, in some cases with

leg symptoms

Nonoperative Care

Rest

NSAID medication

Physical therapy

Steroid injections

Spondylolisthesis


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Surgical care

Failure of nonoperative

treatment

Decompression and fusion

Instrumented

Posterior approach

With interbody fusion

Spondylolysis


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Spondylolysis

Also known as pars defect

Also known as pars fracture

With or without

spondylolisthesis

A fracture or defect in thevertebra, usually in the

posterior elementsmost

frequently in the pars

interarticularis

Spondylolysis


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Symptoms

Low back pain/stiffness

Forward bending

increases pain

Symptoms get worse

with activity May include a stenotic

component resulting in

leg symptoms

Seen most often in athletes

Gymnasts at risk

Caused by repeated strain

Spondylolysis


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Diagnosis

Plain oblique radiographs

CT, in some cases

Nonoperative care

Limit athletic activities

Physical therapy

Most fractures heal without

other medical intervention

Spondylolysis


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Surgical care Failure of nonoperative treatment

Posterior fusion

Instrumented

May require decompression

Ankylosing spondilitis


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optimized by optima


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35. ABDOMINAL INJURIES

Causes


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injuries to theabdomen, pelvis

and genitalia are

generally caused by

accidents involvinghigh kinetic energy

and acceleration or

deceleration forces

Open vs. Closed Injuries


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Abdominal injuries can beeither open or closed

Open injuries are caused by

sharp or high velocity

objects that create an

opening between the

peritoneal cavity and the

outside of the body

Closed injuries are causedby compression trauma

associated with

deceleration forces and

include:

contusions

ruptures

lacerations

shear injuries

The type of injury will depend on whether the organ injured is

Hollow and Solid Organs


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The type of injury will depend on whether the organ injured is

solid or hollow.

hollow organs include:

stomach

intestines

gallbladder

bladder

solid organs

include:

liver

spleen

kidneys

Abdominal Injuries

H ll O I j i S lid O I j i


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when hollow organsrupture, their highlyirritating and

infectious contentsspill into theperitoneal cavity,producing a painful

inflammatory reactioncalled peritonitis

damage to solid organssuch as the liver can causesevere internal bleeding

blood in the peritonealcavity causes peritonitis

when patients injure solidorgans, the symptoms of

shock may overshadowthose from peritonitis

Hollow Organ Injuries Solid Organ Injuries

Abdominal Injuries


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Abdominal injuries canbe obvious, such as an

open wound, or subtle,

such as a blow to the

flank that initiallycauses little pain, but

damages the liver or

spleen

Suspect abdominalinternal injury in any

patient who has a

penetrating abdominal

wound or has sufferedcompression trauma to

the abdomen


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Liver

Largest organ in abdominal After injury blood and bile


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Largest organ in abdominal

cavity Right upper quadrant

Injured from trauma to:

Eighth through twelfthribs on right side of

body Upper central part of

abdomen

Suspect liver injury when:

Steering wheel injury

Lap belt injury

Epigastric trauma

After injury, blood and bile

leak into peritoneal cavity Shock

Peritoneal irritation

Management:

Resuscitation

Laparotomy and repairor resection.

Avulsion of pedicle isfatal


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Stomach/duodenum

Not commonly injured by blunt trauma


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Not commonly injured by blunt trauma

Protected location in abdomen

Penetrating trauma may cause gastric transection or

laceration

Signs of peritonitis from leakage of gastric contents

Diagnosis confirmed during surgery

Unless nasogastric drainage returns blood


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36. ILEUS

Introduction and Definitions

Accounts for 5% of all acute surgical admissions


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Accounts for 5% of all acute surgical admissions

Patients are often extremely ill requiring prompt

assessment, resuscitation and intensive monitoring

Obstructive ileus

A mechanical blockage arising from a structural abnormality

that presents a physical barrier to the progression of gutcontents.

Paralytic Ileus

is a paralytic or functional variety of obstructionObstruction is: Partial or complete

Simple or strangulated

Pathophysiology I

8L of isotonic fluid received by the small intestines (saliva,stomach, duodenum, pancreas and hepatobiliary )


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7L absorbed 2L enter the large intestine and 200 ml excreted in the faeces

Air in the bowel results from swallowed air ( O2 & N2) and bacterialfermentation in the colon ( H2, Methane & CO2),

600 ml of flatus is released

Enteric bacteria consist of coliforms, anaerobes and strep.faecalis. Normal intestinal mucosa has a significant immune role

Distension results from gas and/ or fluid and can exert hydrostaticpressure.

In case of BO Bacterial overgrowth can be rapid If mucosal barrier is breached it may result in translocation of bacteria and

toxins resulting in bactaeremia, septaecemia and toxaemia.

Pathophysiology II

Obstruction results in:1. Initial overcoming of the obstruction by increased paristalsis

I d i l i l b fl id d


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2. Increased intraluminal pressure by fluid and gas

3. Vomiting

4. sequestration of fluid into the lumen from the surroundingcirculation

5. Lymphatic and venous congestion resulting in oedematous tissues

6. Factors 3,4,5 result in hypovolaemia and electrolyte imbalance

7. Further: localised anoxia, mucosal depletion necrosis and perforation

and peritonitis.8. Bacterial over growth with translocation of bacteria and its toxins

causing bacteraemia and septicaemia.

Decompress with NGT

Replace lost fluid Correct electrolyte abnormalities

Recognise strangulation and perforation

Systemic antibiotics.

1. History

The Universal Features


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Colonic

Preexisting change in

bowel habit

Colicky in the lowerabdomin

Vomiting is late

Distension prominent

Cecum ? distended

Distal small bowel

Pain: central and colicky

Vomitus is feculunt

Distension is severe

Visible peristalsis

May continue to pass

flatus and feacus before

absolute constipation

High

Pain is rapid

Vomiting copious and

contains bile jejunal content

Abdominal distension is

limited or localized

Rapid dehydration

Colicky abdominal pain, vomiting, constipation (absolute), abdominaldistension.

Complete HX ( PMH, PSH, ROS, Medication, FH, SH)

Persistent pain may be a sign of strangulation

Relative and absolute constipation

Causes- Small BowelExtraluminalMuralLuminalPostoperativeNeoplasmsF. Body


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adhesions

Congenital

adhesions

Hernia

Volvulus

lipomapolyps

leiyomayoma

hematoma

lymphoma

carcinoid

carinoma

secondary Tumors

Crohns

TB

Stricture

Intussusception

Congenital

BezoarsGall stone

Food Particles

A. lumbricoides

2. Examination

OthersAbdominalGeneral


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Systemic examination

If deemed necessary.

CNS

Vascular

Gynaecologicalmuscuoloskeltal

Abdominal distension

and its pattern

Hernial orifices

Visible peristalsis

Cecal distensionTenderness, guardingand rebound

Organomegaly

Bowel sounds

High pitched

Absent

Rectal examination

Vital signs:

P, BP, RR, T, Sat

dehydration

Anaemia, jaundice, LN

Assessment of vomitus ifpossible

Full lung and heart

examination

Initial Management in the ER

Resuscitate:


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Air way (O260-100%) Insert 2 lines if necessary

IVF : Crytloids at least 120 ml/h. (determined by estimated fluid loss andcardiac function). Add K+at 1mmmol/kg

Draw blood for lab investigations

Inform a senior member in the team.

NPO. Decompress with Naso-gastric tube and secure in position

Insert a urinary catheter (hourly urinary measurements) and start a fluidinput / output chart

Intravenous antibiotics (no clear evidence)

If concerns exist about fluid overloading a central line should be inserted Follow-up lab results and correction of electrolyte imbalance

The patient should be nursed in intermediate care

Rectal tubes should only be used in Sigmoid volvulus.

Indications for Surgery

Immediate intervention:


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Immediate intervention:

Evidence of strangulation (hernia.etc)

Signs of peritonitis resulting from perforation or

ischemia


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37. BURN INJURY

Burn Injuries


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Potential complications Fluid and Electrolyte loss Hypovolemia

Hypothermia, Infection, Acidosis

catecholamine release, vasoconstriction

Renal or hepatic failure

Formation of eschar

Complications of circumferential burn

Burn Injuries

An important step in Thermal burn


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management is todetermine depth andextent of damage todetermine where and howthe patient should be

treated Depth Classification

Superficial

Partial thickness

Full thickness

Skin injury

Inhalation injury

Chemical burn Skin injury

Inhalation injury Mucous membrane

injury

Electrical burn

Lightning Radiation burn

Burn Classifications

1st degree (Superficial burn)


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g ( p )

Involves the epidermis

Characterized by reddening

Tenderness and Pain

Increased warmth

Edema may occur, but noblistering

Burn blanches under pressure

Example - sunburn

Usually heal in ~ 7 days



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2nd degree Damage extends through the

epidermis and involves the dermis.

Not enough to interfere with

regeneration of the epithelium

Moist, shiny appearance

Salmon pink to red color

Painful

Does not have to blister to be 2nddegree

Usually heal in ~7-21 days


3rd degree


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g

Both epidermis and dermis are

destroyed with burning into SC fat

Thick, dry appearance

Pearly gray or charred black color

Painless - nerve endings are destroyed

Pain is due to intermixing of 2nd

degree

May be minor bleeding

Cannot heal and require grafting


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Body Surface Area Estimation


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Rule of Nines Adult

Palm Rule


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38. ARTERIAL DISEASE

Arterial Disease

Raynaud phenomenon is aVasospasm of digital arteries


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vasospastic disease of the digitalarteries; occurs in susceptible

people when exposed to cool

temperatures or during emotional

stress.

Symptoms:

numbness,

paresthesias, or

Pain

Raynaud's syndrome is used to

encompass both the primary &

secondary conditions causing

Raynaud phenomenon.

obliterates the lumen

Inhibited blood flowtriphasic colorresponse

fingers blanch to a distinct white as bloodflow is interrupted

cyanosis, related to local accumulation ofdesaturated hemoglobin

ruddy color as blood flow resumes

Lilly LS. Pathophysiology of heart disease. 5th ed. Lipincott William & Wilkins; 2011.

Brunicardi FC. Schwartz principles of surgery. 8th ed. McGraw-Hill; 2004.

Arterial Disease

Raynaud disease: Raynaud phenomenon:


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Predominantly woman ages 20-40

Mechanism:

sympathetic discharge in

response to cold,

vascular sensitivity to adrenergic

stimuli, or

vasoconstrictor stimuli

(serotonin, thromboxane, &

endothelin)

may appear as a component of otherconditions.

Causes: connective tissue diseases

(scleroderma & SLE) arterial occlusive disorders. carpal tunnel syndrome, thermal or vibration injury.

In patients with connective tissuediseases/arterial occlusive disease: thedigital vascular lumen is largelyobliterated by sclerosis orinflammationlower intraluminal

pressure & greater susceptibility tosympathetically mediatedvasoconstriction.

Treatment:

avoiding cold environments, dressing in warm

clothes, & wearing insulated gloves or

footwear.

Preventing vasospasm with CCB or alpha

blocker.Lilly LS. Pathophysiology of heart disease. 5th ed. Lipincott William & Wilkins; 2011.

39. Urine Incontinence


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Urethral Trauma


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Tanagho EA, et al. Smiths general urology. 17th ed. McGraw-Hill; 2008.

Posterior Urethral Trauma Etiology Pelvic bone fracture

Clinical Symptoms Blood from meatus

Urinary retention Pain, hematom on pubic region

Radiology Pelvic Photo Urethrogram

Therapy Sistostomy Repair 3-4 days later.

41. Pericardial Disease

Etiology of cardiac tamponade:


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neoplastic, postviral, & uremicpericarditis.

Acute hemorrhage intopericardium:

blunt/penetrating chesttrauma,

rupture of the leftventricular free wallfollowing MI,

dissecting aortic aneurysm

Pulsus Paradoxusdecreased of SBP 10 mmHg during inspiration

Thorax expansion duringIn cardiac tamponade, the normal


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inspiration

Intrathoracic pressure becomemore negative

Facilitates venous return &right ventricle filling

Increase in RV size diminishes LV filling

LV stroke volume & systolicblood pressure decline slightly

situation (left diagram) isexaggerated because both ventricles

share a reduced, fixed volume as a

result of external compression by the

tense pericardial fluid.

Pulsus paradoxus may also be

manifested by other conditions in

which inspiration is exaggerated,

including severe asthma & COPD.

McPhee SJ, et al. Pathophysiology of disease. 5th ed. McGraw-Hill; 2006.

Silbernagl S. Color atlas of pathophysiology. 1st ed. Thieme; 2000.Lilly LS. Pathophysiology of heart disease. 5th ed. Lipincott William & Wilkins; 2011.

Cardiac Tamponade

Pericardiosentesis


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Management: ABCs with c-spine control

as indicated

High Flow oxygen

Cardiac Monitor

Large Bore IV access

Rapid Transport

What patient needs is

pericardiocentesis

Using aseptic technique, Insert atleast 3 needle at the angle of the

Xiphoid Cartilage at the 7thrib

Advance needle at 45 degreetowards the clavicle while

aspirating syringe till blood returnis seen

Continue to Aspirate till syringe isfull then discard blood andattempt again till signs of no more

blood

Closely monitor patient due tosmall about of blood aspiratedcan cause a rapid change in bloodpressure


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42. COMPARTMENT SYNDROME

Compartment Syndrome

A condition in which Elevated tissue pressure


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increased pressure withina limited spacecompromises thecirculation and functionof the tissues within thatspace.

within a closed fascialspace

Reduces tissue perfusion

- ischemia Results in cell death -

necrosis

True Orthopaedic Emergency

Compartment SyndromeEtiology


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optimized by optima

Compartment Size tight dressing;Bandage/Cast

localised external pressure;lying on limb

Closure of fascial defects

Compartment Content Bleeding; Fx, vas inj, bleeding disorders

Capillary Permeability;

Ischemia / Trauma / Burns / Exercise / Snake Bite /Drug Injection / IVF


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optimized by optima


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optimized by optima

Compartment SyndromeEtiology

Fractures-closed and Exertional states


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open

Blunt trauma

Temp vascular

occlusion

Cast/dressing

Closure of fascial

defects Burns/electrical

IV/A-lines

Intraosseous IV(infant)

Snake bite

Arterial injury

Compartment SyndromeDiagnosis


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Pain out of proportion

Palpably tense compartment

Pain with passive stretch

Paresthesia/hypoesthesia

Paralysis

Pulselessness/pallor

Clinical Evaluation


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Pain and the aggravation of pain by passive

stretching of the muscles in the compartment in

question are the most sensitive (and generally the

only) clinical finding before the onset of ischemic

dysfunction in the nerves and muscles.


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Compartment SyndromePressure Measurements

Infusion Arterial line


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manometer

saline

3-way stopcock

(Whitesides, CORR1975)

Catheter

wick

slit wick

16 - 18 ga.

Needle

(5-19 mm Hg higher)

transducer monitor

Stryker device

Side port needle

Compartment SyndromeEmergent Treatment

R d i


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Remove cast or dressing Place at level of heart

(DO NOT ELEVATE to optimize perfusion)

Alert OR and Anesthesia Bedside procedure

Medical treatment

Surgical Treatment

F i


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Fasciotomy Casts and tight

bandagesremove or

loosen anyconstricting

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