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1005 > kidney pathophysiology FS > Flashcards

kidney pathophysiology FS Flashcards

1
Q

Name 5 renal disorders

A

postinfectious glomerulonephritis
Polycystic kidney disease
membranous nephropathy
lupus glomerulonephritis
IgA nephropathy
proteinuria
Renal Artery stenosis

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2
Q

Describe the diseased glomerular capillary

A

Sub epithelial deposits as in membranous nephropathy
Large sub epithelial deposits in acute post infectious glomeruleronephritis (Large, irregular subepithelial deposits or “humps”)
Sub-endothelial deposits in diffuse proliferative lupus glomerulonephritis
Mesangial deposits seen in IgA nephropathy
Damage of epithelial foot processes in proteinuria
Autoimmune antibody binding basement membrane(as in Goodpasture syndrome) does not produce visible deposits, but a smooth linear pattern is seen on immunofluorescence)

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3
Q

what is the mesangium composed of

A

mesangial cells surrounded by extracellular matric in direct contact with endothelium

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4
Q

where does ultrafiltration occur

A

across the glomerular wall and through the channels in the mesangial matric into the urinary space

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5
Q

what is the cause of decrease in glomerular filtration rate

A

renal dsease
diabetes
hypertension

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6
Q

what is the cause of decrease in GFR and increase bowmans capusule hydrostatic pressure

A

urinary tract obstruction

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7
Q

what is the cause of increase in glomerular capillary hydrostatic pressure and decrease in glomerular filtration rate?

A

renal blood flow
increased plasma proteins

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8
Q

what is the cause of decrease systemic arterial pressure and decrease in bowmans capusle hydrostatic pressure

A

decrease in arterial pressure

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9
Q

what is the cause of decrease efferent arteoilar resistance and decrease bowmans capsule hydrostatic pressure?

A

angitensin II decrease

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10
Q

what is the cause for increase in afferent arteriolar resistance and a decrease in glomeular capillary hydrostatoc pressure

A

sympathetic activity, vasoconstrictor hormones like nerepinphrine

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11
Q

give two things GFR is determined by

A

balance of hydrostatic qand colloid osmotic forces across the capillary membrane (net filrtation pressure)
Capillary filtration coefficient (Kf), which is the permeability multiplied by the filtering surface area of the capillaries

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12
Q

give the equation to find GFR

A

Kf x net filtration pressure
due to high hydrostatic pressure and Kf, glomerular capillaries have a filtration rate more than other capillaries

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13
Q

how are kidneys classified?

A

acute problems, can stop a kidney function can recover (acute renal failure)

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14
Q

name 4 cause of prerenal acute renal failure

A

intravascular volume depletion
cardiac failure
primary renal hemodynamic abnormalities
peripheral vasodilation and resultant hypotension

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15
Q

what are symptoms of intravascular volume depletion

A

hemorrage
diarrhea
vomit
burns

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16
Q

symptoms of cardiac failure

A

valvular damage
myocardial infarction

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17
Q

symptoms of renal hemodynamic abnormalities

A

embolism
thrombosis of renal artery vein
renal artery stenosis
blockade of prostglandin synthesis

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18
Q

symptoms of peripeheral vasodilation and hypotension

A

anesthesia
anyaphylatic shock
sepsis
severe infection

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19
Q

In Europe, the most commonly prescribed NSAIDs are:

A

diclofenac
ibuprofen
naproxen
celecoxib
mefenamic acid
etoricoxib
indomethacin
aspirin (in doses greater than 600mg

20
Q

What are NSAIDs

A

Non steroidal anti inflammatory drugs
they block prostaglanding synthesis
they inhibit COX-2 enzymes in the kidney

21
Q

What is the function of prostoglandin in the kidney?

A

PGI2,PGE2, thromboxane A2(TXA2), and PGF2αare made there

PGs affect vascular tone (increase RBF) and NaCl transport

PGI2&PGE2stimulates renin and aldosterone release

22
Q

In the macula densa what happens when increase flow and na+ delivery occurs

A

ATP is released
decrease GFR maintains normal filtered load
decreases renin secretion allows more NA+ secretion

23
Q

In the macula densa what happens when decrease flow and na+ delivery occurs

A

NO and prostoglandins produced
increase GFR maintains normal filtered load
increases renein secretion and conserves NA+

24
Q

What can prostoglandin oppose

A

oppose ADH
helps in water excretion

25
Q

name some vasoconstrictors

A

angiotensin II
vasopressin
endothelin
catecholamines

26
Q

Name some vasodilaters

A

prostoglandins
nitric oxide

27
Q

what are the risk factors asociates with nSAIDS and getting acute renal failure

A

vomit
old age
diarrhoes
true intravscular volume depletion
diuretics
cirrhosis

28
Q

what is chronic renal disease

A

gradual loss of function and irrerversible loss of mnay nephrons
high prevalence

29
Q

causes of chronic renal failure

A

metabolic disorders
renal vascular disrders
infections
immunological disorder
primary tubular disordere
congenital disorder
urinary tract obstruction

30
Q

describe the vicious cycle of primary kidney disease

A

loss of nephrons
causes hypertrophy and vasodilation of nephrons so increase arteial pressure which injsures capillaries and flow
increase in glomeular pressure and filtration
causes glomelular sclerosis/loss

31
Q

main 2 causes of end stage renal disease

A

diabetes
hypertension

32
Q

what are the disorders of renal physiology

A

tubule functions
neurological or endocrine control

33
Q

what are tubule functions

A

damage to renal epithelial cells, disruption to solute transporters

34
Q

what is wrong with the function of neurological or endocrine control

A

neuronal pathology
endocrine pathologies, abnromal hormone levels/receptor defects

35
Q

how are renal defects detected and treated

A

patient experiences lain and infection and chnages in urinary behavior and collur
urine flow rate
prescence of proteins eg: albumins/blood or foregin material in urine
abnormal ion, creatinine clearance

36
Q

how are renal defects treated

A

treat primary cause, high bp, cvd
control tubular functions or diruesis

37
Q

list the common symptoms of renal disease

A

Fluid changes (increased blood volume)
Electrolyte changes (hyperuricemia, hyperkalaemia)
Neuromuscular (fatigue, headache, lethargy)
CVS/RS (pulmonary oedema, heart failure)
Skin (pallor)
GI (nausea & vomiting)
Blood (e.g. anaemia)

38
Q

name ten chemicals that majorly affect public health

A

air pollution
arsenic
asbestos
benzene
cadium
dioxin
flouridelead
mercury
pesticides

39
Q

how is meatal exposure measured in humans

A

occupational exposure: to general public
metal concentrations in blood, urine, hair +fingernails
renal pathology: metals in urine/tissue+ measurements of renal function

40
Q

name the routes of exposure

A

inhalation
diet
drinking water
skin
medical proedures/ devices

41
Q

how the inc/dec renin, and angiotensin/aldosterone occur

A

decrease in GFR
decrease in flow to loop of henle
inc in NaCl reabsorption in ascending limb
decrease in NacCl in distal tube
inc of renin

42
Q

what leads to over production of aldosterone

A

diabetes

43
Q

name two milestones with transplants of kidneys due to diabetes

A

pakistans first cadaver organ transplant
first locally harvested cadaver organ transplant

44
Q

what conditions lead to diluting urine

A

central diabetes insipudus= ADH not release/made due to congenital defects trauma or infection
patients excrete up to 15l/day of dilute urin, no major changes in body fluid is fluid is taken
nephrogenic diabetes inspidus= ADH is normal by kidneys dont respond. lots of dilute urine

45
Q

what is nephrogenic diabetes insipus due to

A

defective ADH receptors
defective aqaporin water channels in collecting duct
drug side effects
no hyperosmotic medulla due to renal disease

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