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SAQs > Mechanisms > Flashcards

Mechanisms Flashcards

1
Q

cirrhosis to portal hypertension?

A
  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
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2
Q

cirrhosis to haemtemisis

A

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

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3
Q

cirrhosis to ascites

A

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

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4
Q

hypovolemia to increased resp rate

A

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

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5
Q

IgA nephropathy to hypoalbuminism

A

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

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6
Q

Iga nephropathy to hypertension

A

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

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7
Q

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

A

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

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8
Q

pathogenesis of MS

A

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

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9
Q

hyperthyroid to oligomenorrhea

A

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

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10
Q

hyperthyroid to increase RR

A

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

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11
Q

hypercortisolism to nocturia

A

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

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12
Q

hypercortisolism to back pain

A

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

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13
Q

pituitary adenoma to hirustism

A

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

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14
Q

hypercortisolism to leukocytosis

A

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

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15
Q

hypercortisolism to bruising/red striae

A
  1. immune suppression > impaired healing ability.

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

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16
Q

hypercortisolism to tachpnea

A

increased sensitivity to catecholamines and angiontensin II > tachypnea

17
Q

hypercortisolism to muscle weakness

A
  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
18
Q

hypercortisolism to hypertension

A
  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
19
Q

T1DM to vomitting

A

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

20
Q

T1DM to weight loss with increase appetite

A

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

21
Q

2ndary athsma stimulus to airway obstruction

A

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

22
Q

pulsus paradoxus

A
  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
23
Q

1st exposure to asthma stimulant

A

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

24
Q

athsma attack to collapse

A

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

25
Q

TB droplet to Granuloma

A

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

26
Q

Latent TB to 2ndary infection with symtoms

A 
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

SAQs (13 decks)

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