Mechanisms

Question 1

cirrhosis to portal hypertension?

Answer 1

1. Hepatic vein is directly compressed by regenerating nodules
2. Small portal vein branches are trapped, narrowed and distorted by scar tissue
3. Hepatic arterial blood (which is naturally higher than venous pressure) shunts to portal vein via arteriovenous anastomoses.
   All these lead into portal hypertension

Question 2

cirrhosis to haemtemisis

Answer 2

cirrhosis> portal hypertension > anastamosis causes varice at oesophagus > varice bleeds > haemtemisis

Question 3

cirrhosis to ascites

Answer 3

cirrhosis> portal hypertension > increase hydrostatic pressure > fluid in cavity.
Cirrhosis > decrease liver function > decrease albumin > hpyoalbuminemea > decrease oncotic pressure > odema

Question 4

hypovolemia to increased resp rate

Answer 4

hypovolemia> decreased blood blood to kidneys > acute tubular necrosis > loss of tubular function > decrease H+ excretion and decrease bicarb reabsorption > metabolic acidosis > increased RR

Question 5

IgA nephropathy to hypoalbuminism

Answer 5

deposits of IgA in glomeruli> immune mediated sclerosis of glomeruli > inncrease in pore size of basement membrane + decrease neg charge > proteins able to filter through > albumin excreted in urine > hypoalbuminaemia

Question 6

Iga nephropathy to hypertension

Answer 6

deposits of IgA in glomeruli> immune mediated sclerosis of glomeruli > reduction in GFR > renin released from juxtaglomerular apparatus > activates angiotensin II > vasoconstriction, cardiac myocyte hypertrophy > increase CO and MAP > hypertension.

*could also add excess fluid not secreted from decrease GFR. and ADH + aldosterone from RAAS

Question 7

head trauma to all elements of cushings reflex (hypertension, bradycardia and irregular RR)

Answer 7

head trauma > intracranial bleeding > raised ICP > pushes on brainstem (irregular breathing/LOC).
Raised ICP> activation of SNS > vasoconstriction + tachycardia > increase in BP > baroreceptors respond > parasymapthetic activation > bradycardia

Question 8

pathogenesis of MS

Answer 8

CD4 T cell reacts to myelin Ag > activates TH1 (which then activates isotype switching in B cells), Th17, astrocytes and microglia> increase permeability in BBB > inflammation causes damage/destruction to myelin > appearance of legions

Question 9

hyperthyroid to oligomenorrhea

Answer 9

increase BMR of all cells > decrease in adipocytes > liver synthesizes more SHBG > decrease sex hormones > suboptimal LH surge > oligomenorrhea

Question 10

hyperthyroid to increase RR

Answer 10

increase BMR of all cells > increase cellular respiration > increase in CO2 and decrease in O2 > increase RR

Question 11

hypercortisolism to nocturia

Answer 11

increase gluconeogenisis and peripheral decrease glucose uptake > increase blood and urine glucose > noctouria and thirst

Question 12

hypercortisolism to back pain

Answer 12

increase osteoclast activity > decrease bone density > fracture in lumbar vertabrae

Question 13

pituitary adenoma to hirustism

Answer 13

increase ACTH release > increase stimulation of zona fasiculata (and reticularis) > increase in androgen production > hirusuitism and oligomenorrhea

Question 14

hypercortisolism to leukocytosis

Answer 14

increase neutrophil release from bone marrow and decrease neutrophil adhesion molecules.
immune suppression lead to lymphocytopaenia but neutrophillia outweighs

Question 15

hypercortisolism to bruising/red striae

Answer 15

1. immune suppression > impaired healing ability.

2. increase peripheral lipolysis and decrease collagen synthesis > thinning of skin > increased brusing/ red striae

Question 16

hypercortisolism to tachpnea

Answer 16

increased sensitivity to catecholamines and angiontensin II > tachypnea

Question 17

hypercortisolism to muscle weakness

Answer 17

1. Increase protein catabolim (for gluconeogenisis)> muscle weakness
2. mimics aldosterone by binding to its receptor in distal tubule > increased K secretion into tubule > hypokalaemia > muscle weakness

Question 18

hypercortisolism to hypertension

Answer 18

1. increase sensitivity to SNS > vasoconstriction and increase heart rate > increase CO and MAP > hypertension.
2. cross-reactivty with minarelcorticoid receptor in kindey mimics aldosterone > Na and water retention > increase blood volume > increase EDV > increase SV > increase BP

Question 19

T1DM to vomitting

Answer 19

destruction of islet beta cells > decrease insulin production > decrease glucose uptake > increase fatty acid oxidation > ketoacidosis > vomit

Question 20

T1DM to weight loss with increase appetite

Answer 20

destruction of islet beta cells > decrease insulin production > decrease glucose uptake > increase protein catabolism for energy > weight loss and polyphagia

Question 21

2ndary athsma stimulus to airway obstruction

Answer 21

antigen IgE crosslinking on Mast cells > 3 stage response (immediate - histamine, rapid - prostaglandins + luekotrienes, late -cytokines) > bronchoconstriction, mucus secretion, vasodilation and oedema > airway obstruction

Question 22

pulsus paradoxus

Answer 22

1. decreaes intrathoracic pressure during inspiration > increase venous return > RV enlarges> pushes septum into LV > decrease filling.
2. ecreaes intrathoracic pressure during inspiration> lungs expand > pulmonary vasculature expands > blood pools in lungs > decrease LV filling > decrease SV = lower systolic pressure

Question 23

1st exposure to asthma stimulant

Answer 23

antigen interacts with APC > lymphatics > stimulates TH2 cells > invokes B cell isotype switching to IgE > sensitises IgE receptors on mast cells to antigen

Question 24

athsma attack to collapse

Answer 24

airway obstruction > decrease ventilation > Ventilation perfusion mismatch > hypoxia > decrease Hb saturation > lack of oxygen to brain > collapse/confusion

Question 25

TB droplet to Granuloma

Answer 25

inhalation of droplet containing mycobacteria (most likely mycobacterium tuberculosis) > ingestion by alveolar macrophage > bacteria resist killing and slowly divide intracellulary > macrophages present antigen which stimulates TH1 cells > TH1 release IFN-gamma > IFN-gamma causes differentiation to epithelioid macrophages and may fuse to form giant cells > Activated macrophages secrete TNF which promotes recruitment of more 
monocytes > formation of granuloma with caseous necrosis core contains bacteria > lymphocytes surround granuloma

Question 26

Latent TB to 2ndary infection with symtoms

Answer 26

``` immune suppression (infection, stress, lack of sleep, smoking, malnutrition) > TB reactivated > pulmonary infection (usually apical lobe due to higher concentration of oxygen) > macrophages release IL 1, TNF > fever > night sweats > fatigue. Productive cough from neutrophilia ```