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Renal > More Kidney - drugs > Flashcards

More Kidney - drugs Flashcards

1
Q

ADPKD

A

Autosomal dominant polycystic kidney disease

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2
Q

ADPKD genes

A

PKD 1 encodes polycystin 1 - chromosome 16. Dialysis by 53

PKD 2 encodes polycystin 2, chromosome 4, layer dialysis. LEss common

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3
Q

Pathophysiology of ADPKS

A

PC1 complexes with PC2 - regulates PC2 channel activity. If apical cilia bends, complex activated, calcium influx and CAMP activated - increased sensitivity of CD to ADH. CFTR gene also inclides.

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4
Q

PKD1 types`

A

Can be truncating or nontruncating, truncating is more prevalent and severe

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5
Q

Kidney size class

A

1a-1e, bigger kidneys increase PCKD risk and indicates prognosis

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6
Q

Associated conditions in ADPCKD

A

Cerevral aneurysms, liver cysts (but no impaired function), abdo aortic aneurism, diverticular disease, bronchiectassi, LV hypertrophy, mitral valve prolapse

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7
Q

Genetic risk?

A

Autosomal dominant, but needs two hits, so some people will not develop cysts. Screening not recommended, but U/S cyst detection is prognostic. Can also use MRI (need more cysts on MRI to diagnose)

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8
Q

ADPCKD Tx

A

Good BP control (<110/75), doesn’t affect GFR but does give smaller kidneys. Often use ACEi/ARB (but in women of childbearing, consider CCBs/diuretics). Tolvaptan (ADH inhibitor, reduces AQP2 and cAMP). - ADEs, thirst, polyuria, nocturia, headache, dry mouth). Can mimic tolvaptan by drinking lots of water

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9
Q

Bartter’s syndrome

A

Affects Na/K/2CL in ALoH - leads to hypomagnesia, hypocalcaemia. PRevents infancy/prenatal. Severe lack of concentrating capacity, GFR may be normal or declining.

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10
Q

Gitelman’s

A

Affects thiazide (Na/Cl) in DCT. Causes hypomagnesaemia. Urine calcium excretion may be reduced. Concentrating capcity normal or slightly impaired. GFR normal.

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11
Q

OAT

A

Organic acid transporters. Used for uric acid, drugs etc. Active transport with Tm

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12
Q

OCT

A

Organic cation transporters. Facilitated diffusion. DA, choline, drugs transport

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13
Q

Dose adjustment importantin KD when:

A

CRCl<50ml/min
Drug >50% renally excreted
Drug with NTW
Age

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14
Q

Effect of urea on BBB

A

Increases permability so increased sensitivity to drugs in CNS in renal impairment

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15
Q

AKI definition?

A

a) increase in SCr within 48h
b) Increase in SCr 1.5x baseline in 7 days
c) URine volume <0.5mL/Kg/H) in adults for 6+ hours
d) Decrease in eGFR

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16
Q

Prostaglandin effect on GFR?

A

Normally vasodilate afferent arteriole, increasing GFR. Therefore NSAID block of PG can decrease GFR

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17
Q

Angiotensin effect on GFR

A

Vasoconstricts. Predominantly on efferent arteriole, but higher ANG II causes both to constrict (although efferent constricts more to maintain GFR)

Therefore, ACEi/ARBs can decrease GFR

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18
Q

CKD -EPI

A

Sex, SCr, age, ethnicity and formula changes depedning on Creatinine range (accommodates nonlinear GFR/Creatinine relationship)

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19
Q

Parameters affecting cystatin C

A

Smoking, inflammation, corticosteroids, diabetes, obesity, thyroid

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20
Q

Small Vd drug kidney disease effects

A

If dehydrated, drugs with small Vd will be more affected and have increased plasma concentration

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21
Q

Where is urea secreted by UT-A2

A

DLoH

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22
Q

Ammonia secreted by 2GP /rhesus transporters?

A

CD

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23
Q

Diuretics causes photosensitivity?

A

Thiazides and loop

24
Q

Diuretic causing decreased glucose tolerance?

A

Thiazide

25
Q

Diuretic causing tinnitus/deafness

A

Frusemide at high dose, long period

26
Q

Halflife equation

A

T1/2 = 0.693/K

27
Q

Hw much of body is water

A

55-60%

28
Q

Water proportions

A

2/3 is ICP, 1/3 is ECP (and 20% of this is plasma)

29
Q

Osmolality is, osmolarity is

A

Solute/Kg (mOsmol/Kg) - osmometer (est. 2x Na)

Solute/L, calculate from Na/K/urea/glucose

30
Q

tonicity is

A

taking into account only non-penetrating substances - looks at water movement due to substances drawing water towards them

31
Q

Urine osmolarity

A

300mOsm/L, same as plasma

32
Q

Where is urea reabsorbed

A

CD by UT-1 and UT-2 (under ADH control), allows concentration of urine

33
Q

ADH released by

A

Supraoptic /paraventricular nuclei of thalamus. Stored in post pit.

34
Q

ADH stimulated by

A

If osmolality increases, hypothalamic osmoreceptors (anterior 3rd ventricle, near supraoptic nuclei) shrink - >signal to post pit for ADH release.
Can also be stimulated by baroreceptor, decreased atrial stretch (carotid sinus) and JGA receptors as well as pain, hypoxia, emesis, exercise, hypoglycaemia, nausea, morphine, nicotine, cholinergic agonist, beta blocker, angiotensin and prostaglandins

35
Q

ADH inhibitors

A

alcohol, alpha blocker, glucocorticoids

36
Q

thirst disorders

A

Polydipsia (?psychogenic), hypodipsia (thirst deficiency or unable to access fluid, hypernatraemia risk), adipsia (rare, ?trauma)

37
Q

ADH dysfunction includes

A

DI (central or nephrogenic), SIADH (often tumour based)

38
Q

Potassium homeostasis needed for

A

Muscle strength, heart rate. In hyperkalaemia, see tall tented T wave, broad WRS (before CA). In hypokalaemia, see small, flat T wave, prominent U wave.

39
Q

Things that drive hyperkalaemia

A

Na/K/ATPase inhibition (e.g. hypoxia), trauma/infection, cell lysis, severe exercise, rhabdomylosis, beta blockers, hyperglycaemia (sugar draws water out of cell and potassium follows)
Also, in acidosis, H+ can exchange for K+ and so K+ moves out of cell

40
Q

Things that drive hypokalaemia

A

Insulin (causes uptake into sleletal muscle and liver), catechoamines, epinephrine, (therefore debta 2 activation causes uptake)

41
Q

Hyperkalaemia treatment can involve:

A

Beta 2 agonist, alklaine fluid, insulin

42
Q

Pseudohyperkalaemia

A

mishandled blood sample

43
Q

Potassium reabsorption

A

Unregulated (paraceullar solvent drag) in PCT, also in DCT by intercalated cells (alpha)
Also in Na/K/2Cl pump in ALoH

44
Q

Potassium secretion

A

DCT and CD principal cells (ROMK, also
MAXIK in CD)
ROMK influenced by aldosteron as Aldosterone enhances ENAC, so Na/K/ATPase works harder and therefore more potassium secretion.

45
Q

Relationship between K+ and proton excretion

A

If plasma potassium low, more potassium reabsorbed into intercalating cell in exchange for hydrogen secretion, therefore alkalosis.
In acodisos, more hydrogen secreted leading to more potassium reabsorption

46
Q

5 Step Tx of hyperkalaemia

A

1) stabilise heart (10mL,10% calcium gluconate)
2) dextrose with insulin
3) correct acidosis (bicarb)
4) increase excretion (correct hypovolaemia, loop diuretic, consider dialysis)
5) reduce potassium (can also use binders - > sodium zirvonium, patiromer)t

47
Q

U&E in hypovolaemia

A

may have elvated urea (normal creatinine), urine concentrated

48
Q

Causes of hyponatraemia

A

1) dehyration. If renal loss then high urine Na (think diuretics, or AddisonsIf low Na then extra renal (burns, sepsis etc)
2) Oedema, body perceived hypovolaemia (urine low sodium as RAAS activated)
3) Euvolaemia (e.g. hypothyroidism, psychogenic polydipsia (low urine osmolality) and SIADH (high urine osmolality))

49
Q

Addisons

A

No aldosterone (or cortisol), causes hyponatraemia, hyperkalaemia, hypotension, hypoglycaemia and pigmentation (ACTH)

50
Q

SIADH

A

Can be lung or brain pathology. Diagnosis is no oedema, reduced plasma osmolality, inaproproate urine osmolality for serum (>300), high urine sodium, normal acid/base/potassium/adrenal/thyroid function, no renal impairment.
Can be post op, lung neoplasm, medication induced. Manage by fluid restriction and tolvaptan

51
Q

Conn’s diease

A

Hyperaldosteronism. Fluid overload

52
Q

Danger of hasty hyponatraemia correction

A

Central pontine myelinosis (permanent pons injury)

53
Q

Diabetes insupidus

A

ADH issue, either central or nephrogenic. Polyuria and polydipsia.

54
Q

Net glomerulus filtration pressure

A

GBHP(blood) - CHP(hydrostatic) - BCOP (coloid oncotic)

55-15-30 = 10mmHg

55
Q

Tubulointerstitial disease

A

Lsck of urine concentrating ability. Urine shows low osmolality, protein/RBCs absent, high sodium. Renal biopsy not used.
Do get casts (ATN), eosinophils(AIN).
Will also get 10:1 BUN: Cr

56
Q

ATN

A

Ischaemic, hypoperfusion of kidney (esp tubular cells). Causes azotaemia, uraemia (mental status change, oedema, fatigue, N&V). Dx by urine low osmolality, high sodium, muddy brown casts (tubular endothelial cells). Assess potassium, ECG if high. Tx - monitor, dialysis if severe

57
Q

AIN

A

Allergic interstitial nephritis.
Often caused by drugs (allopurinol, penicillin, cephalosporins, quinolones, rifampin, sulfas), also autoimmune (SLE) and infections.
Presents with fever, rash, WBC in urinalysis. FBC shows eosinophilia. Urine oesinophils (Hansel’s stain).
Remove stimulus to treat (+/- steroid)

Renal (6 decks)

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