Past questions Flashcards
A 60 year old man with symptoms/risk factors of coronary heart disease has a transmural MI. 4 days later he suddenly develops shortness of breath, orthopnoea, hypertension and is found to have pulmonary oedema (has bilateral basal creps).
Give 3 causes for his pulmonary oedema
Increased capillary hydrostatic pressure caused by:
fluid overload from LV dysfunction, mitral regurg from MI ripping papillary muscles , hospital acquired pneumonia
Mechanism for breathlessness, pulmonary oedema, orthopnea & pansystolic murmur after MI
MI > LV dysfunction > increase pulmonary capillary hydrostatic pressure > oedema> decreased lung compliance> increase WOB .
MI > LV dysfunction > increase pulmonary capillary hydrostatic pressure > increase WOB > SOB.
Gravity when lying causes blood to pool in pulmonary circulation when lying down > increase pulmonary pressure > SOB.
murmur = MI > mitral regurgitation (common after inferior MI) > pansystloic murmur.
or IHD > LV hypertrophy > mitral Regurg > murmur
or LV failure > fluid build up in lungs > RV failure > tricuspid regurg > murmu
Describe how a PA chest radiograph is systematically assessed?
What would you expect patients’s to look like
From inside to out. Start with midline - Trachea (midline shift), spine, heart. Check that the heart to chest ratio is no more than half. Check the the lung hilum for increases in diameter pressure or lymph enlargement.
Then check lungs for fluid > check pleura >
Then thoracic wall and soft tissue > then diaphragm.
Would expect this patient to have Kerley B lines due to his pulmonary oedema. And most likely an enlarged heart as it is likely his MI was caused by coronary heart disease
4 causes for chronic renal failure?
diabetic nephropathy, hypertension, glomerularnephritis, drugs
skeletal bone damage in Chronic renal failure
the hypocalcaemia and hyperphophataemia induce hyperparathyroidism. The increase in PTH increases osteoclast activity, extracting calcium from bone to compensate. this makes the bones weaker and more likely to fracture
Hyperphosphatemia & hypocalcemia in renal failure
hyperphosphotaemia due to decreased ability of kidneys to excrete phsophate.
Hypocalcaemia due to decrease ability of kidneys to produce vitamin D3 (as it makes one of the enzymes in the process). Vitamin D3 increases calcium absorption from gut, calcium renal reabsorption and increases osteoclast activation.
Causes of secondary hypertension
Chronic renal failure > decreased fluid excretion > fluid overload > increase BP.
Renal Artery Stenosis > low GFR > RAAS > vasoconstriction, cardiac hypertrpophy, Aldosterone production > increase MAP
Role of the juxtaglomerular apparatus in GFR
juxtaglomerular apparatus responds to:
- Direct Sympathetic stimulation
- changes in renal perfusion pressure (detected directly by the granular cells)
- changes in NaCl concentration at the macula densa.
structures in danger in hemithyoidectomy? where are they and what are potential problems
parathyroid glands (2 sets of gland, superior + inferior on posterior surface of each lobe of thyroid gland).
Recurrent Laryng -
para will cause hypocalcaemia + hyperphosphataemia. nerve damage can cause hoarse voice or loss of voice. May also cause resp issues by paralysising the cricoartynoid muscle which opens vocal cords.
thyroid hormone to increase HR meachanism
Increase Thyroid hormone> sympathomimetic effect increases b1 adrenorecptors on SA node> increase HR
why does thyroid mass move on swallowing?
firmly connected to the larynx by the pre-tracheal fascia. when swallow the inferior constrictor muscle constricts moving the larynx up and down
thyroid hormone production
TSH binds to follicular cell > stimulates thyrglobulin synthesis in rough ER> thyroglobulin enters colloid by exocytosis > I- enters via NIS symport > Thyroid perioxidase oxidises I- to I > Iodine is added by enzymes to tyrosine to make MIT or with MIT to make DIT > DIT + DIT = T4 or DIT + MIT = T3 > taken back into follicular cell via endocytosis > enzymes separate T3 and T4 from protein into bloodstream
Difference between normal anxiety for anxiety about medical procedures?
Blood-injury phobias differ from all other phobias in that the initial sympathetic activity underpinning the flight/fight response is soon overtaken by vagal activation. Thus, initially there may be a transient rise in heart rate and blood pressure, however, this is followed my marked vasovagal slowing of heart rate, a drop in blood pressure, there is nausea, sweating and pallor, and the individual may faint.
It is worth noting that people without a blood phobia also also show vagal inhibition in response to blood-injury stimuli despite sympathetic activation. Thus individuals with blood-injury phobias differ in the degree of cardiovascular response to blood or injury, rather than the type.
Outline the pathogenesis of hepatitis/cirrhosis. Make reference to specific cells.
Cirrhosis is the conversion of the liver into a state of abnormal anatomy= nodules of regenerating heptocytes surrounded by bands of fibrous (scar tissue). It is the end stage of all chronic hepatitis.
Pathology of cirrohsis includes chronic/ persistant hepatocyte necrosis, extracellular matrix deposition (fibrosis, or scar tissue formation), remodelling of the liver vascular supply (thought to be important in the later progression of cirrohosis)
The main source of abnormal collagen is the stalite cells. Stalite cells become activated – they contract and produce collagen (they turn into myofibroblasts).cytokines from the kupfler cells activates stalite cells.
How does alcohol cause damage to hepatocytes?
The main effects of alcohol on the liver are inflammation coupled with the accumulation of fat. Histological features are hepatocellular ballooning, mallory bodies and percellular fibrosis
The accumulation has 3 key mechanisms:
1) shunting of normal substrates away from catabolism and toward lipid synthesis, as a result of increased NADH (biproducts of ADH and AHDH).
(2) impaired assembly and secretion of lipoproteins.
(3) increased peripheral catabolism of fat, thus releasing free fatty acids into the circulation.
According to Robbins the causes of inflammation “are uncertain” but the ROS as a result of Cytochrome P 450 metabolism plays a role as it reacts with proteins, damages membranes and alters cellular function.
