CVS patho and pharmaco

Question 1

lymph node in the neck (or some other part of the body) shows metastatic squamous carcinoma, what likely organs did it come from?

What is the most impt feature in the histology that suggests squamous origin?

Answer 1

a. Skin, lungs etc
b. keratin pearls

Question 2

practical approach to lymph node enlargement
a. if u suspect lymphoma
b. if u suspect infection

Answer 2

a. FNAC
b. biopsy

Question 3

patient presents with mediastinal lymphadenopathy of the lung. Think of?

Answer 3

Hodgekin’s lymphoma!!

Question 4

how to find source of primary tumour in patient with secondary neoplasms in lymph nodes?

Answer 4

1. immmunohistochemistry, molecular signals
2. clinical features like site of lymph node enlargement, consider organs in proximity
3. histological characteristics

Question 5

which is correct about indolent lymphoma?
1. have a long median survival
2. usually have high mitotic rate
3. display prominent nucleoli
4. usually curable

Answer 5

1. have a long median survival

indolent lymphomas, unlike aggressive lymphomas, proliferate slowly but has defective apoptosis. Low mitotic rate, nucleoli not prominent (coz low mitotic rate so low rate of dna replication, not active), widespread by the time it is diagnosed, long median survival.

defective apoptosis means not curable unless rare limited disease

Question 6

on autopsy, the gross appearance of the aorta is recorded and compared with the microscopic findings of the atheroma formation. Which of the following is most likely the first visible gross evidence for the formation of an atheroma?
1. ulcerated plaque
2. fibrous cap
3. fatty streak
4. thrombus formation

Answer 6

fatty streak (C)

fatty streak happens first then fibrous cap then ulcerated plaque and lastly thrombus formation

Question 7

what are the 4 clinical consequences of acute plaque change?

Answer 7

rupture, fissure, erosion, ulceration, hemorrhage

1.cerebral infarction
2. myocardial infarction
3. aortic aneurysm
4. peripheral vascular disease

Question 8

what are 5 the chronic atherosclerotic stenosis?

Answer 8

1. stable angina
2. chronic ischaemic heart disease
3. bowel ischaemia
4. ischaemic encephalopathy
5. intermittent claudication

Question 9

what are the GENERAL consequence of atherosclerosis and how does the pathophysiology of the CONSEQUENCES work?

Answer 9

ischemia, aneurysm rupture haemorrhage, thrombosis

vessel thickening, narrow lumen, decreased tissue perfusion hence ischemia

loss of elasticity, predisposition to aneurysm, rupture and haemorrhage

endothelial damage when plaque ruptures and exposes sub-endothelium which is a pro-thrombotic layer, predisposes to thrombosis

Question 10

define atheroma

Answer 10

atheroma refers to lesions in tunica intima resulting in plaque consisting of a raised lesion with a soft, yellow core of lipid covered by a white fibrous cap.

Question 11

10 year old boy found unresponsive by his mother. A week before, he had sought treatment for sore throat and fever. Autopsy shows Aschoff bodies in myocardium. Which is the most likely cause of death?
1. infective endocarditis
2. streptococcal sepsis
3. aortic dissection
4. myocarditis
5. encephalitis

Answer 11

myocarditis

aschoff bodies seen in acute RHD which causes pancarditis.
Myocarditis is part of pancarditis.

streptococcus may cause RHD but is not the cause of death. It is RHD that causes pancarditis and pancarditis causes the death uk wat i mean

Question 12

which of the following gross or histological features are least likely to be present in the CVS system of someone with benign hypertension?
1. smaller lumen
2. hyaline deposits
3. fibrinoid necrosis of the vessel wall
4. thrombotic microangiopathy
5. renal tubular necrosis

Answer 12

ans: C
benign hypertension: hyaline arteriosclerosis
malignant: hyperplastic arteriosclerosis, where it is associated with fibrinoid necrosis of the vessel wall

Question 13

adverse effects of cholestyramine

Answer 13

1. GI effects like nausea, constipation, flatulence
2. impaired absorption of fat soluble vitamin ADEK which can lead to night blindness, osteoporosis and blood disorders

Question 14

mode of action of statins

Answer 14

statins like simvastatin, atorvastatin are HMG-CoA reductase inhibitors which are involved in the RATE LIMITING STEP of cholesterol synthesis, hence reducing cholesterol synthesis.

depletion of intracellular cholesterol will cause an increase in LDL receptor production hence increase uptake of plasma LDL

Question 15

Pharmacokinetics of statins and which part of the day should it be given

Answer 15

oral administration with first pass extraction\
given in the evening!!

Question 16

which lipid lowering drug has fibrinolytic properties?

Answer 16

Niacin. it decreases circulating fibrinogen and increases tissue plasminogen activator and hence reverses thrombosis associated hypercholesterolemia and atherosclerosis

while we are at it, niacin also strongly inhibits lipolysis in adipose tissues. plasma triglyceride VLDL and cholesterol LDL is lowered.

niacin also increases HDL-cholesterol levels

Question 17

which lipid lowering drug adverse effects involves hyperuricemia and gout?

Answer 17

niacin

Question 18

pt physical examination
- Bp 80/40 HR 130bpm
-SpO2 85%
-restless, unable to lie down flat
-cool peripheries
-JVP elevated to angle of jaw
- HS S1 S2, no murmur heard
- Lung bibasal crepitation
- pedal edema

what is the heart failure clinical profile?

(hint: dry/ wet/ warm/ cold etc)

Answer 18

JVP elevation to angle of jaw , tachypoiec, bibasal crepitations, pedal edema suggests congestion
hence wet

cool peripheries, low bp, restlessness suggests hypoperfusion hence cold

hence cold and wet

actually the diagnosis is severe cardiogenic shock secondary to myocarditis so pt has to be intubated and mechanically ventilated.
circulation: intra-aortic balloon pump insertion, inotropic support, VA ECMO for 5 days

Question 19

1Diuretics- thiazides acts on DCT. what is the MOA?
what is it indicated for and explain more about it

this will be tested

Answer 19

inhibits NaCl reabsorption by blocking Na/Cl- transporter. Enhances Ca2+ reabsorption in DCT

indicated for hypercalcicuria

thiazides causes a decrease in concentration of sodium in tubular cells hence enhance Na+/Ca2+ exchanger activity, creating an increased drive for Ca2+ reabsorption through apical/epithelial Ca2+ channels

Question 20

how is thiazides indicated for nephrogenic diabetes insipidus?

Answer 20

nephrogenic DI-> low/no response to ADH, water reabsorption in collecting duct decreases, urine increases. Body water decreases hence NaCl conc increases, increasing osmotic pressure, causing thirsty dehydration and pt to drink more water so that extracellular volume increases and GFR increases.

Thiazides (diuretics) increases NaCl excretion, hence decreased NaCl conc in the body, decreasing osmotic pressure, no thirsty dehydration, wont drink more water hence extracellular vol. decreases, decrease GFR and at the same time increase proximal reabsorption of water. This decreases delivery of fluid to DCT and collecting tubule, decreasing urine output

Question 21

which of the following is the least likely cause of left-sided heart failure?
1. patent foramen ovale
2. hypertension
3. ischaemic heart disease
4. aortic stenosis

Answer 21

patent foramen ovale
- similar to atrial septal defect which is classified under L2R shunt, right sided HF.

Question 22

pt is a neonate with large ventricular septal defect. the cardiologist recommends early surgical closure of the defect because

1. there is a L2R shunt which results in cyanosis and risk of death
2. this will lead to pulmonary hypertension and right ventricular hypertrophy
3. there will be insufficient blood reaching the systemic circulation
4. stress on the heart will lead to acute MI
5. circulation is dependent on the ductus arteriosus, which will close soon after birth

Answer 22

2.

recall pulm. htn anf rv hypetrophy will lead to pulm circulation pressure reaching systemic circulation pressure levels, then will lead to R2L shunt aka shunt reversal

Eisenmenger syndrome pathway

Question 23

describe the 3 different pathogenesis of aneurysm

Answer 23

1. ischemia
2. Degradation of collagen by local inflammation (in atherosclerosis and vasculitis; activation of matrix metalloproteinases or tissue inhibitor of metalloproteinase)
3. poor intrinsic quality of the vascular wall connective tissue (e.g. Marfan syndrome, Vitamin C deficiency)

Question 24

name 2 examples of congenital heart diseases not associated with significant shunting of blood

Answer 24

aortic stenosis (bicuspid valve)
coarctation of aorta

Question 25

name 3 disorders that might predispose to cor pulmonale

Answer 25

disease of pulm parenchyma (COPD, diffuse pulm interstitial fibrosis, pneumoconioses, cystic fibrosis, bronchiectasis)

diseases of pulm vessels (saddle embolus, recurrent pulm thromnoembolism, extensive pulm arteritis, primary pulm hypertension)

disorders inducing pulmonary arterial constriction (metabolic acidosis, hypoxaemia, chronic altitude sickness, sleep apnea, obstruction of major airways)

disorders affecting chest movements (kyphoscoliosis, marked obesity)

Question 26

what are the 5 possible complications of AMI?

Answer 26

arrhythmias (just think when tissue dies, electrical conductivity interrupted, or when cardiac cells lack oxygen, become depolarised, altered impulse conduction)
rupture and hemorrhage (hemopericardium, caridac tamponade)

papillary muscle dysfunction
thrombus
aneurysms
progressive HF

Question 27

what is the pathological effects of HTN on CNS and kidney?

Answer 27

CNS
- hypertensive encephalopathy
- cerebral hemorrhage
- cerebral thrombosis

kidney
- hardening of small blood vessel in kidney hence nephrosclerosis

Question 28

possible fates of thrombus

Answer 28

dissolution
organisation and recanalisation
propagation
embolism

Question 29

what are the pathological effects of HTN heart?

Answer 29

LHF
also leads to cor pulmonale
chronic heart failure eventually

ans: hypertensive heart disease whereby LV pressure overload, LV hypertrophy, impaired LV diastolic filling, LA dilatation, LV failure

Question 30

how does the treatment differ for fresh thrombus and organized thrombus?

Answer 30

fresh thrombus: dissolve thrombus using anti-thrombotics and TPA (tissue plasminogen activator)

organised thrombus: coronary bypass/ angioplasty and healthy lifestyle

Question 31

IVDA usually is causes what valve disease?

Answer 31

IVDA results in staph aureus infection causing ACUTE infective endocarditis; affecting mitral valve, followed by aortic valve

Question 32

which of the following is a complication of tertiary syphilis?
1. aortic stenosis
2. aortic regurg
3. mitral stenosis
4. mitral regurg
5. pulm regurg

Answer 32

aortic insufficiency aka aortic regurg

Question 33

what is not seen in cor pulmonale?
1. primary pul. hypertension
2. pulm valve stenosis
3. sleep apnea
4. chronic parenchymal disease
5. recurrent pulm embolism

Answer 33

Pulm valve stenosis!
ans: 2

recall disorders that predisposes to cor pulmonale (which is RV structure alteration and dysfunction caused by primary disorder of the resp system)

1. disease of the pulm parenchyma (COPD, cystic fibrosis, bronchiectasis)
2. disease of pulm. vessels (saddle embolus, recurrent pulm thromboembolism, primary pulm HTN, extensive pul. arteries)
3. disease including pulm. constriction (metabolic acidosis, chronic altitude sickness, sleep apnea, obstruction of major airways)
4. disease affecting chest movements (kyphoscoliosis, marked obesity)

REJECTED: pulm valve stenosis (this is a heart valve dysfunction, dont get trick just because you see the word pulmonary in it!!)

Question 34

ok this qn is fucking gay but uk that acute infective endocarditis e.g. IVDA, open heart surgery, septicaemia

then IVDA usually is by staph aureus right…

and IE most common valve affected is mitral valve followed by aortic valve

can be regurg or stenosis but not prolapse!

(recall mitral prolapse leads to mitral regurg ok)

so what valve is affected in IVDA?

Answer 34

TRICUSPID VALVE!!!!!