CVS patho and pharmaco Flashcards
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?
a. Skin, lungs etc
b. keratin pearls
practical approach to lymph node enlargement
a. if u suspect lymphoma
b. if u suspect infection
a. FNAC
b. biopsy
patient presents with mediastinal lymphadenopathy of the lung. Think of?
Hodgekin’s lymphoma!!
how to find source of primary tumour in patient with secondary neoplasms in lymph nodes?
- immmunohistochemistry, molecular signals
- clinical features like site of lymph node enlargement, consider organs in proximity
- histological characteristics
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
- 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
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
fatty streak (C)
fatty streak happens first then fibrous cap then ulcerated plaque and lastly thrombus formation
what are the 4 clinical consequences of acute plaque change?
rupture, fissure, erosion, ulceration, hemorrhage
1.cerebral infarction
2. myocardial infarction
3. aortic aneurysm
4. peripheral vascular disease
what are 5 the chronic atherosclerotic stenosis?
- stable angina
- chronic ischaemic heart disease
- bowel ischaemia
- ischaemic encephalopathy
- intermittent claudication
what are the GENERAL consequence of atherosclerosis and how does the pathophysiology of the CONSEQUENCES work?
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
define atheroma
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.
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
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
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
ans: C
benign hypertension: hyaline arteriosclerosis
malignant: hyperplastic arteriosclerosis, where it is associated with fibrinoid necrosis of the vessel wall
adverse effects of cholestyramine
- GI effects like nausea, constipation, flatulence
- impaired absorption of fat soluble vitamin ADEK which can lead to night blindness, osteoporosis and blood disorders
mode of action of statins
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
Pharmacokinetics of statins and which part of the day should it be given
oral administration with first pass extraction\
given in the evening!!
which lipid lowering drug has fibrinolytic properties?
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
which lipid lowering drug adverse effects involves hyperuricemia and gout?
niacin
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)
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
1Diuretics- thiazides acts on DCT. what is the MOA?
what is it indicated for and explain more about it
this will be tested
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
how is thiazides indicated for nephrogenic diabetes insipidus?
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
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
patent foramen ovale
- similar to atrial septal defect which is classified under L2R shunt, right sided HF.
pt is a neonate with large ventricular septal defect. the cardiologist recommends early surgical closure of the defect because
- there is a L2R shunt which results in cyanosis and risk of death
- this will lead to pulmonary hypertension and right ventricular hypertrophy
- there will be insufficient blood reaching the systemic circulation
- stress on the heart will lead to acute MI
- circulation is dependent on the ductus arteriosus, which will close soon after birth
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
describe the 3 different pathogenesis of aneurysm
- ischemia
- Degradation of collagen by local inflammation (in atherosclerosis and vasculitis; activation of matrix metalloproteinases or tissue inhibitor of metalloproteinase)
- poor intrinsic quality of the vascular wall connective tissue (e.g. Marfan syndrome, Vitamin C deficiency)
name 2 examples of congenital heart diseases not associated with significant shunting of blood
aortic stenosis (bicuspid valve)
coarctation of aorta
