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PBLs > Week 14 - Renal > Flashcards

Week 14 - Renal Flashcards

1
Q

what is the function of the kidneys?

A

regulate the volume and osmolality of the extracellular fluid by altering the amount of soidum and water excreted

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2
Q

what is the function of ADH and where does it bind?

A

ADH binds to receptors on plasma membrane of collecting duct cells
causes increase in amount of aquaporins
increases permeability to water
more water reabsorbed
more concentrated urine

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3
Q

where is ADH released from?

A

posterior pituitary

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4
Q

what happens in the glomerulus?

A

hydrostatic pressure in the glomerulus is higher than in the bowmans capsule so fluid is forced out of the blood into the glomerular filtrate via ultrafiltration.

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5
Q

what happens in the proximal convoluted tubule?

A

Selective reabsorption of all the glucose, amino acids and most of the water happens in the proximal convoluted tubule.

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6
Q

what happens in the loop of henle?

A
  • The descending limb is permeable to water but impermeable to salts (Na+, Cl-)
  • The ascending limb is permeable to salts but impermeable to water
  • Descending limb: water is lost from filtrate by osmosis as it moves from a higher water potential in the filtrate to a lower water potential in the medulla -> moves into blood
    Ascending limb: at the very bottom some salts diffuse out as the filtrate is very concentrated, after this salts are actively transported out, giving the filtrate a higher water potential again
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7
Q

what happens in the distal convoluted tubule?

A

Excess ions are added and those needed by the body are reabsorbed

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8
Q

what happens in the collecting duct?

A
  • More water is lost from the filtrate by osmosis as the collecting duct descends into the medulla (High WP to low WP).

The amount of water reabsorbed at this stage is controlled by the number of aquaporins in the collecting duct (increased by anti-diuretic hormone (ADH) binding to specific membrane bound receptors and activating a series of enzyme controlled reactions, which results in the formation of vesicles with many water permeable channels AKA aquaporins)

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9
Q

what lab tests can assess kidney function?

A

Blood tests
eGFR– creatinine is a waste product that is filtered and not reabsorbed by the kidneys. Creatine clearance is a useful evaluation of GFR. Estimated Glomerular Filter Rate – an estimation of how much waste the kidneys can filter in a minute. The results are categorised into 5 stages, with stage 1 being normal and stage 5 meaning the kidneys have lost almost all of their function.

Urine Tests
* Used to check the albumin:creatinine ratio (ACR). The results are classified into 3 stages.
* Check for blood or protein in the urine

Other tests
* Ultrasound scan, MRI scan or CT scan to check what the kidneys look like/assess for damage
Kidney biopsy

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10
Q

when in renin released from the kidney?

A

in response to low BP and low fluid volume

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11
Q

what is the action of renin?

A

acts on angiotensinogen to form angiotensin 1

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12
Q

what converts angiotensinogen to angiotensin 1?

A

renin

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13
Q

what is the action of ACE in the renal system?

A

converts angiotensin 1 to angiotensin 2

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14
Q

what converts angiotensin 1 to angiotensin 2?

A

ACE

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15
Q

where is ACE release?

A

lungs

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16
Q

where does angiotensin 2 act and what does it do?

A

adrenal gland = stimulates release of aldosterone

blood vessels = stimulates vasoconstriction

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17
Q

where does aldosterone act and what does it do?

A

on kidneys to stimulate reabsorption of salt and water

* Increase sodium reabsorption from the distal tubule
* Increase potassium secretion from the distal tubule Increase hydrogen secretion from the collecting ducts
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18
Q

where is aldosterone released from?

A

adrenal glands

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19
Q

what type of hormone is aldosterone?

A

mineralocorticoid steroid hormone

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20
Q

where is angiotensinogen released from?

A

liver

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21
Q

how are the kidneys involved in acid-base balance?

A

kidneys maintain the acid-base balance by two mechanisms - the cells reabsorb bicarbonate HCO3 from the urine back to the blood and they secrete hydrogen (H+) ions into the urine.

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22
Q

what 3 hormones are released by the kidneys?

A

erythropoitin
calcitriol
renin

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23
Q

what is the function of erythropoietin?

A

Binding of the hormone to receptors on the membrane of red blood cell precursors reduces apoptosis

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24
Q

what is the function of calcitriol?

A
  • Final activation of vit D to the active calcitriol occurs in the kidneys
    • Calcitriol stimulates the small intestine for protein synthesis allowing absorption of Ca2+ and phosphate
    • This ensures the availability of Ca2+ and phosphate for bone growth
      Calcitriol simultaneously activates osteoblasts to synthesise collagen
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25
Q

what is the NICE criteria for an AKI?

A
  • Rise in creatinine of ≥ 25 micromol/L in 48 hours
  • Rise in creatinine of ≥ 50% in 7 days
    Urine output of < 0.5ml/kg/hour for > 6 hours
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26
Q

what are the risk factors of an AKI?

A
  • CKD
  • Heart failure
  • Diabetes
  • Liver disease
  • Age (>65)
  • Cognitive impairment
  • Use of contrast medium e.g. CT scans
    Nephrotoxic medications - NSAIDs, ACE inhibitors
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27
Q

what medications need to be stopped in an AKI?

A

NSAIDS
ACEi

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28
Q

what are the 3 types of causes of an AKI?

A

prerenal - most common cause of AKI, inadequate blood supply to kidneys reducing filtration of blood

renal - intrinsic disease in kidney –> reduced filtration of blood

post-renal - obstruction to outflow of urine from kidney, causing back-pressure into kidney –> reduced kidney function (obstructive uropathy)

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29
Q

what are some prerenal causes of AKI?

A
  • Dehydration
    • Hypotension (shock)
    • Heart failure - any failure e.g. liver etc
    • NSAIDs/ACEi - affect tone of afferent/efferent arteriole
      Renal artery stenosis
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30
Q

what are some renal cuases of an AKI?

A
  • Glomerulonephritis
    • Interstitial nephritis
      Acute tubular necrosis - due to pre-renal AKI - common
31
Q

what are some postrenal causes of an AKI?

A
  • Kidney stones
  • Masses such as cancer in the abdomen or pelvis
  • Ureter/ureteral strictures
    Enlarged prostate or prostate cancer
32
Q

what are some clinical signs of an AKI?

A
  • Oliguria or anuria
  • Signs of hypovolaemia: dry mucous membranes, reduced skin turgor, tachycardia, hypotension
  • Signs of volume overload: hypertension, pulmonary oedema, peripheral oedema, elevated jugular venous pulse
  • Signs of uraemia: ecchymosis due to platelet dysfunction, uraemic encephalopathy (e.g. asterixis, confusion, seizures)
  • Signs of post-renal obstruction: palpable or tender distended bladder
33
Q

what is seen of urinalysis during AKI?

A

○ Protein, blood - suggest acute nephritis (can be positive in infection)
○ Leucocytes, nitrites - suggests infection
Glucose - suggests diabetes

34
Q

what is the management of an AKI?

A

stop nephrotoxic medications and IV fluids

treat underlying cause

35
Q

what is diabetic nephropathy?

A

The chronic high level of glucose passing through the glomerulus causes scarring. This is called glomerulosclerosis.

common cause of glomerular pathology and CKD

· Hyperglycaemia leads to increase in growth factors, renin–angiotensin–aldosterone activation, production of advanced glycosylation end-products, and oxidative stress.
This causes increased glomerular capillary pressure, podocyte damage, and endothelial dysfunction

36
Q

what are some clinical signs of diabetic nephropathy?

A

albuminuria
glomerulosclerosis
nodule formation
fibrosis

37
Q

how is diabetic nephropathy diagnosed?

A

*** proteinuria - damage of glomerulus allows proteins to be filtered through

Microalbuminuria (‘moderately increased albuminuria’) = A:CR 3–30mg/ mmol (p294, 302). Regression at this level of disease is possible. Not detected on standard dipstick, must send A:CR.

38
Q

how do diabetics have regular screening for diabetic nephropathy?

A

testing the albumin:creatinine ratio and U&Es.

39
Q

what is the management for diabetic nephropathy?

A

· Treatment is by optimising blood sugar levels and blood pressure.

· ACE inhibitors are the treatment of choice in diabetics for blood pressure control. They should be started in patients with diabetic nephropathy even if they have a normal blood pressure.

· Sodium restriction to <2g/day

Statins to reduce CVD risk.

40
Q

what is oliguria?

A

low urine output
* In adults this is <400ml to 500ml of urine per 24 hours.
In children this is <0.5ml/kg/hr

41
Q

what are some causes of oliguria?

A
  • Pre-renal causes:
    ○ Low blood volume → this can be caused by heavy blood loss, decreased fluid intake, burns, sepsis, liver failure and surgery
    ○ Heart and lung conditions
    ○ Vascular disease of your kidneys
    • Renal causes:
      ○ Glomerulonephritis
      ○ Acute tubular necrosis
      ○ Damage due to medications or toxins
    • Post-renal causes:
      Blockages in urinary tract → bladder outlet obstruction, ureteral stones
42
Q

how is oliguria treated?

A
  • Blockages → can be removed
    • Infection → treat with antibiotics
    • Drug that has damaged the kidneys → stop medication and replace it
      Dehydration → drink fluids or get IV fluids
43
Q

what is polyuria?

A

when your body produces too much urine, >3 litres a day for adults

44
Q

what are the symptoms of polyuria?

A
  • Excretion of > 3litres is considered to be abnormal
    • Polyuria is often coupled with polydipsia
      Frequent urination, especially at night (nocturia)
45
Q

what are some causes of polyuria?

A
  • Kidney failure
    • Diabetes mellitus
    • Diabetes insipidus
    • Diuretic medications
    • Lithium
    • Alcohol or caffeine intake
      Pregnancy
46
Q

what are some complications of an AKI?

A
  • Hyperkalaemia
    • Fluid overload, heart failure, pulmonary oedema
    • Metabolic acidosis
      Uraemia (high urea) → lead to encephalopathy or pericarditis
47
Q

what are some causes of CKD?

A
  • Diabetes
    • Hypertension
    • Age-related decline
    • Glomerulonephritis
    • Polycystic kidney disease
      Medications → NSAIDs. PPIs. Lithium
48
Q

what are some risk factors of CKD?

A
  • Older age
    • Hypertension
    • Diabetes
    • Smoking
      Use of medication that affects the kidneys
49
Q

what is the presentation of CKD?

A

→ usually asymptomatic. A number of signs and symptoms might suggest CKD:
* Pruritus
* Loss of appetite
* Nausea
* Oedema
* Muscle cramps
* Peripheral neuropathy
* Pallor
Hypertension

50
Q

what investigations suggest CKD?

A
  • eGFR → two tests required 3 months apart fo confirm diagnosis
    • Proteinuria → checked using a urine ACR; result of >3 mg/mmol is significant
    • Haematuria → checked using a urine dipstick; significant result is 1+ of blood.
      Renal ultrasound → used to investigate patients with accelerated CKD, haematuria, family history of polycystic kidney disease or evidence of obstruction
51
Q

what is needed to confirm a CKD diagnosis?

A
  • eGFR → two tests required 3 months apart fo confirm diagnosis
52
Q

what are some complications of CKD?

A
  • Anaemia
    • Renal bone disease
    • Peripheral neuropathy
      Dialysis related problems
53
Q

what is dysuria?

A

Pain, discomfort, or itching in the urethral meatus when urinating

54
Q

where is renal pain felt?

A

lower back and loin

55
Q

what are some causes of dysuria?

A

infective
* infections or urethritis
* Pyelonephritis
* Prostatitis
* vaginitis
sexually transmitted diseases

non-infective
skin conditions
* foreign body or stone in the urinary tract
* trauma
* benign prostatic hypertrophy
* Tumors
* interstitial cystitis
* Medications
* specific anatomic abnormalities
* Menopause
reactive arthritis

56
Q

what is the action of loop diuretics?

A

Inhibit the reabsorption of Na+ (and .: water) at the Loop of Henle
- Inhibit the NaCl transporter

57
Q

where do loop diuretics act?

A

loop of henle

58
Q

when can loop diuretics be used?

A
  • Pulmonary oedema
  • Heart failure
  • Renal insufficiency
  • Resistant hypertension
59
Q

what are some side effects of loop diuretics?

A
  • Hypovolaemia
  • Hyponatremia
  • Hypotension
  • Hypokalaemia
    Metabolic alkalosis
60
Q

what are some examples of loop diuretics?

A
  • Furosemide
  • Bumetanide
    Terasemide
61
Q

what is the action of thiazide diuretics?

A

inhibit the reabsorption of Na+ (and .: water) at the beginning of the distal convoluted tubule
Inhibit the NaCl transporter

62
Q

where do thiazide diuretics act?

A

distal convoluted tubule

63
Q

what are some side effects of thiazide diuretics?

A
  • Frequent urination (polyuria)
  • Hypokalaemia
  • Erectile dysfunction
  • Hypovolaemia
    Hyponatraemia
64
Q

what are some examples of thiazide diuretics?

A

Originals
* Chlorothiazide (oedema + HTN)
* Hydrochlorothiazide
* Bendroflumethiazide (HF)

Thiazide-like
* Indapamide (HTN)
* Chlorthalidone
Metolazone

65
Q

what is the action of aldosterone antagoinists?

A

Block the effect of aldosterone .: inhibits the reabsorption of Na+ (and .: water) at the collecting duct

66
Q

where do aldosterone antagonists act?

A

collecting duct

67
Q

what are the clinical uses of aldosterone antagonists?

A
  • Heart failure
  • Hyperaldosteronism (Conns)
    Resistant hypertension (particularly with low renin)
68
Q

what are some examples of aldosterone antagonists?

A
  • Spironolactone
    Eplerenone
69
Q

which diuretics cause hypokalaemia and which cause hyperkalaemia?

A

hypo = loop and thiazide
hyper = aldosterone antagonists

70
Q

what triad of side effects do both loop and thiazide diuretics have?

A

hypokalaemia
hyponatraemia
hypovoaemia

71
Q

which diuretics cause erectile disfucntion?

A

thiazide

72
Q

which diuretics cause metabolic alkalosis?

A

loop

73
Q

what should always be assessed when taking diuretics?

A

U+Es
can cause electrolyte disturbances
Particularly aldosterone antagonists need renal function assessing as the cause hyperkalaemia

PBLs (19 decks)

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