Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

IPAP Biochem Thompson > Urinary > Flashcards

Urinary Flashcards

1
Q

Function of nephron?

A 
Acid 
Water balance
Electrolyte balance
Toxin removal
Bp control
Erythropoietin
D vitamin
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Renal corpuscle blood pathway?

A

Afferent arteriole-glomeruli (filtered)-leaves efferent arteriole - peritubular capillaries - vasa recta - renal vein

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Fenestrations?

A

Endothelial lining w/ neg charged “openings”

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What can get through fenestrations?

A

Anything smaller than an RBC

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Glomerular basal lamina layers?

A
  • Lamina rara interna
  • Lamina densa
  • Lamina rara externa
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

GLomerular basal lamina purpose?

A

-3 layers for efficient and highly selective sieve-like filter

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Where in glomerular basla lamina do you find glycosaminoglycans?

A

-The lamina rara interna and lamina rara externa

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What glucosaminglycans are found in glomerular basal lining?

A

Heparin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Lamina densa composition?

A

-Filamentous type 4 collagen (kinked sheet pattern)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What is the glycoprotein laminin?

A

Cross links that bind type 4 collagen in the glomerular basal lamina

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Podocytes?

A

Specialized epithelial cells covering the basement membrane of the glomerulus in the kidney.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What lines and stabilizes the slit diaphragms (podocytes)

A

-Podocin, nephrin (proteins), and glycocalyx (neg charged glycoprotein)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Minimal change disease?

A
  • Nephropathy (defect in podocin)

- Loss of podocyte foot processes -> proteinuria -> and water imbalance -> edema

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

JAG?

A

Juxtaglomerular apparatus - regulates function of each nephron

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Mesangial cells?

A

Modified smooth muscle cells in glomerulus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Messangial cells functions?

A

-Regulate blood flow->affterent caps

Produce extracellular proteins

Phagocytically remove filatration (filter and clean)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What synthesizes, stores, and secretes the enzyme renin?

A

JAG cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Antiglomerular basement antibody disease?

A

Good pastures syndrome

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Goodpastures syndrome vs alport’s syndrome?

A

Goodpastures-autoimmune

Alport’s- Genetic mutation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Good pastures syndrome?

A
  • Autoimmune attacks type 4 collagen of basal lamina of glomeruli and alveoli -> inflammation of glomeruli
  • Rapidly progressive glomerular nephritis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Alports syndrome?

A
  • Genetic mutation of type 4 collagen-deposition of IgG

- Leads to inflammatory destruction of the glomeruli (glomerulonephritis)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

PCKD?

A

Polycystic kidney disease

-Inherited disorder-noncancerous cysts develop w/in kidneys, round sacks containing water-like fluid

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Non-proliferative glomerular disorders?

A
  • minimal change glomerulonephritis
  • focal segmental glomerulosclerosis
  • Hereditary glomerulonephritis (alports syndrome)
  • IgA nephropathy (bergers disease)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Proliferative glomerular disorders?

A
  • HEnoch-schonlein purpura
  • Membranoproliferative glomerulonephritis
  • Goodpastures syndrome and wegners granulomatosis
  • Postinfectious glomerulonephritis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Diabetic neuropathy?

A
  • Progressive thinking of glomerular structure w/ destruction of glomeruli
  • Increasing protein in urine
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Regions of the nephron?

A

PCT
Loop of Henle
DCT
Collecting duct

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Nephron anatomy?

A
  • Glomerulus:filters blood
  • PCT:reabsorbs ions, water, nutrients, removes toxins, adjusts pH
  • Descending loop:aquaporins; water->ISF
  • Ascending loop:reabsorbs Na+ and Cl- into ISF
  • Distal tubule: secretes+absorbs ions to maintaining pH and electrolytes
  • Collecting duct: reabsorbs solutes and water.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Where is water absorbed?

A

PCT, LOH, Collecting duct (Aquaporin 2)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Glucose reabsorption?

A

Urine side-> SGLT1/2 -> GLut 1/2 -> blood side

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

High serum glucose affect on urine?

A

-Down regulates GLUTE and indirectly inhibits SGLT-> keeps glucose in urine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

Resorption of AA, proteins, and peptides?

A

-99% reabsorption via molecule-specific channels in PCT

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

Sodium reabsorption?

A

PCT
thick ascneding loop
DCT
Collecting duct

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

Where is most/least sodium reabsorbed?

A

65% NA/K/ATPase channgel in PCT

5% aldosterone-regulated Na/k channels in colelcting duct

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

K reabsorption?

A

65% passive diffusion PCT

20% LOH

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

Cl- reabsorption?

A
  • Passive channels in PCT
  • Sodium potassium chloride co-transporter in LOH
  • Sodium potassium chloride co-transporter in DCT
36
Q

What allows the exchange of chloride ions for bicarb ions in the nephrons?

A

The Cl/HCO3 exchanger

37
Q

What is CIC-5?

A

-Chloride channel in renal tubules critical for normal tubular function

38
Q

HCO3 reabsorption?

A

80-90% in the PCT

39
Q

How much urea filtered in the glomeruli is found in urine?

A

40%

40
Q

Where does the largest portion of uerea reabsorption occur?

A

50% occurs via passive transport channels in PCT

41
Q

What drives reabsorption of Ca2+ and PO43 in the DCT?

A

Vitamin D and PTH = Ca2+

Vitamin D=PO43

42
Q

Best way to measure GFR?

A
  • Most accurately measured by insulin

- Most practical=blood creatine (from muscle breakdown of creatine phosphate)

43
Q

GFR normal vs CKD5 failure?

A

Normal= 90ml/min with proteinn in urine

Failure= 15ml/min (1/6th of normal)

44
Q

Where does the RAAS start?

A

JAG apparatus

45
Q

DEfine RAAS?

A
  • Renin-angiotensin-aldosterone system

- Regulatory pathway involving kidney, liver, lung, adrenals, pituitary gland, and selected arterioles (kidney)

46
Q

What is the macula densa and how does it work?

A

Regulates blood volume using Na+ and gaseous NO

47
Q

What causes renin to be secreted?

A

-Changes in arteriole BP activate special nerve cells in JAG (macula densa) -> JAG cells releases renin

48
Q

Where dfoes renin fit into the RAAS?

A

REnin is an enzyme that acts on angiotensinogen -> angiotensinogen I

49
Q

What are Renin inhibitors?

A

-Block the conversion of angiotensinogen -> angeotensin I, treating high BP

50
Q

How do macula densa cells work?

A
  • High Na levels (osmolarity is high) overwhelms the macula densa
  • High Na and osmotic gradient ->macula densa swelling
  • Swelling activates stretch activated channels allowing atp to escape
  • ATP is converted into adeonsine
  • Adenosine receptors allow for constriction of afferent and dilation of efferent arterioles
  • Slows down GFR, converting less urine -> decrease in Na concentration decreasing macula densa swelling
51
Q

NOS?

A

Nitric oxide synthase activated by low blood flow through glomules

52
Q

Macula densa summary?

A

High Na->densa swelling->release ATP/adenosine->vasoconstriction

Low Na->densa NOS activation -> vasodilation

53
Q

Angiotensinogen pathway?

A

-Angiottensinogen+renin->angiotensinn 1+ACE-Angiotensin II + aminopeptidase - angiotensin III+angiotensinases - degradation of product

Raise BP

54
Q

WHere do ACE inhibitors work?

A

-STOPS ACE FROM converting angiotensin I - Angiotensin II

55
Q

Angiotensins II effect on heart?

A

Vasoconstriction

Raise BP

56
Q

Angiotensin II effect on brain?

A

Increased ACTH by pituitary

Raise BP

57
Q

Avoiding ACE sifde effects?

A

use angiotensin receptor blocker class of meds

ARB

58
Q

Mineralcorticoids action?

A
  • maintain blood volume/BP by increasing Na+ reabsorption in DCT
  • INcreased Na+ -> excretion of K+ and protons H+ leading to reabsoption of water
59
Q

What is the primary mineralcorticoid?

A

Aldosterone

60
Q

Action of aldosterone?

A

Binds to mineralcorticoid receptors in DCT->upregulation of Na+/K+ pumps (ATP dependent basolateral pumps)

Concentrates Na+ in interstitium -> more Na+ in blood and more K+ in urine

61
Q

What are ENaCs?

A

Epitheal sodium channels - upregulated by aldosterone w/ increasing apical membrane (Facing the lumen) permeability for Na+

62
Q

Conn syndrome?

A

-Overproduction of aldosterone

Higher BP and metabolic alkalosis

63
Q

Addisons disease?

Acidons disease

A

Underproduction of aldosterone

Low BP and metabolic acidosis

64
Q

Potassium sparing diuretics and aldoesteron regulation?

A

Competitive inhibitor for aldosterone receptors in collecting duct -> blocks effects (membrane permeability and # of Na-K pumps) -> decreasing Na and H2O reabsorption but keeping more K

65
Q

Vasopressin aka ADH?

A

Affects H2O content by urine by affecting aquaporin-2 channels

66
Q

Defects of AQ2 channels?

A

Aquaporin2 channel defects cause water loss (pts w/ nephrogenic diabetes insipidous) or water retention (pregnancy/congestive heart failure)

67
Q

Diabetes insipidus 2 types?

A

Nephrogenic diabetes insipidus-mutations of AQ2 channel

Neurogenic central diabetes insipidus-no vasopressin (hypthal or pituitary gland failure) - tumors, trauma

68
Q

Types of natriuetic peptides?

A

ANP- atrial natiuretic peptide

BNP- Brain natriuretic peptide

69
Q

Naturietic peptides function?

A

Opposite of aldosterone- released when H blood volume/BP

70
Q

Proposed medical use for ANP/BNP ?

A

Treating CHF

71
Q

Normal pH range?

A

7..35-7.45

72
Q

Respiratory vs metabolic acid base balance mechanisms?

A

Respiratory-pulmonary expiration of CO2

Metabolic- kidney elimination of HCO3, H+

73
Q

Carbonic anhydrase?

A

Enzyme that affects intercalated cells (both H+ and HCO3 secreting)

74
Q

Increased blood acidosis causes?

A

REabsorption of HCO3 from PCT, LOH, and Collecting duct back into blood

Secretion of H from collecting duct

75
Q

Increased blood alkalosis causes?

A

Decreted H secretion

Less resorption (more secretion) of HCO3

76
Q

Metabolic acidosis info

A

PH <7.35
HCO, pCO are low

Causes-diabetic ketoacidosis; lactic acidosis

Compensation - Hyperventilate excrete CO2

77
Q

Metabolic alkalosis info?

A

Ph >7.45
HCO, pCO HIGH
Causes-vomiting
Compensation-hypoventilation-retention of CO2

78
Q

Respiratory acidosis info?

A

Ph <7.35
HCO, PCO high
Causes- COPD, resp muscle paralysis
Compensation- retention of HCO, increased H secretion

79
Q

Respiratory alkalosis info?

A

Ph >7.45
HCO, pCO LOW
Causes anxiety; acute pain
COmpensation - excretion of HCO, decrease H secretion

80
Q

Hyperammonemia?

NH3 toxicity

A

Free NH3 = toxic to nervous system

81
Q

What can Noxic ammonia do to our body?

A

Mental retardation, seizures, uncontrolled muscle movements, breathing irregularities, poor control of body temp

82
Q

Erythropoietin?

A

Glycoprotein cytokine and hormone that regulates production of RBCs

83
Q

Where is EPO made?

A

Kidneys

Peritubular capillaries

In endothelial cells

84
Q

What enzyme is needed for one of the final steps of vitamin D synthesis?

A

1-a-hyroxylase in the PCT (25-hydroxyvitamin d2 1-alpha-hydroxylase

85
Q

Kidney stone types+causes?

A

Calcium oxalate-H oxalate in urine+Ca2+= stone
Uric acid- increase uric acid in urine makes uric acid stones
Struvite ammonium magnesium phosphate -urea splitting bacteria raises acidity and makes stones
Calcium phosphate-hyperPTH makes more ca and phos which makes stones

Cystine-defect transport channel in PCT -> H cystine (acid) -> cystine stones

IPAP Biochem Thompson (4 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions