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GU > Nephro 1 > Flashcards

Nephro 1 Flashcards

1
Q

What are the main functions of the kidney?

A

Filter and secrete waste/excess

Retain albumin and circulating cells

Reabsorb glucose, amino acids and bicarb

Control BP, fluid status and electrolyes

Activates 25-hydroxy Vit D –> 1,25 dihydroxy vitamin D (calcitriol)

Synthesis erythropoietin

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2
Q

What is the glomerular filtration rate?

A

Volume of fluid filtered from the glomeruli into Bowman’s space per unit time

120ml/min

7.2L/h

170L/day

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3
Q

What are characteristics of PCT?

A

Proximal Convoluted tubule

sugars, amino acids and bicarbonate get reabsorbed here

70% of Na+ absorbed and water follows

MOST vulnerable to damage

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4
Q

What is Fanconi syndrome?

A

not to be confused with FANCONI ANAEMIA

Proximal tubule insult (Wilson’s, tenofovir)

  • glycosuria
  • acidosis
  • phosphate wasting = rickets/osteomalacia
  • aminoaciduria
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5
Q

What are the functions of the loop of henle?

A

25% of Na+ absroved here and water follows

Thiazide diuretics work here

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6
Q

What are the functions of the distal convoluted tubule?

A

The juxtaglomerular apparatus

  • a solute sensing organ, if it detects HIGH SOLUTES - GFR is low = releases RENIN
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7
Q

What are the actions of Renin?

A
  1. It converts angiotensinogen to angiotensin-I
  2. ACE from lungs converts angiotensin 1 to 2
  3. This causes vasoconstriction and release of aldosterone
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8
Q

What are functions of the collecting duct?

A

salt handling, tightly regulated by aldosterone (increases reabsorption of Na+ in exchange for K+)

Secrete K+ and H+ into the urine

Water handling is also done here via Aquaporin 2 channels (these regulated by vasopressin)

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9
Q

How is potassium handled by the kidney?

A

K+ freely filtered and mostly reabsorbed in PROXIMAL TUBULE/LOOP OF HENLE

Governed by Na+ and Aldosterone

Insulin and catecholamines drive K+ uptake

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10
Q

What drugs cause hypokalaemia?

A

Loop diuretics and thiazide diuretics

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11
Q

What drugs cause hyperkalaemia?

A

spironolactone

amiloride

ACE-I

ARB

Trimethoprim

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12
Q

What is urinating regulated neurally?

A

S3,4,5 via parasympathetic - contract detrusor relax urethra

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13
Q

How is storage of urine regulated neurally?

A

T10, L1, L2 via sympathetic nervous system - RELAX bladder CONTRACT urethral sphincter

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14
Q

What are the 3 main narrowings where renal stones can lodge themselves?

A

Pelviureteric Junction

Pelvic Brim

Vesicoureteric Junction

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15
Q

What are most renal stones made of?

A

Calcium oxalate and Phosphate

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16
Q

What are some risk factors for renal stones?

A

Anatomical abnormalities

Chemical composition of urine that favours stone crystallisation

Dehydration

Infection

Increased Ca, Oxalate, Urate

Primary renal disease

Drugs - diuretics, antacids, acetazolamide, corticosteroids

Chocolate, rhubarb

Gout

Fam Hx

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17
Q

How would renal stones/renal colic present?

A

Asymp

Renal Colic - rapid onset, loin to groin, comes and goes in waves, nausea and vomiting, worse with fluid loading

Dysuria, strangury (burning when peeing), frequency

Recurrent UTI’s

haematuria

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18
Q

How would you investigate renal colic?

A

Urinalysis - maybe normal, exclude other causes

FBC - WBC to rule out infection

Serum electrolytes, urea and creatinine - hypercalcaemia, hyperuricaemia

Urine pregnancy test - ectopic

non-contrast CT

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19
Q

How would you treat renal stones/colic?

A

Conservative - overhydration, low Ca, dietary intake, low sodium, reduced BMI, reduced animal proteins

Morphine

Ondansetron

Abx - trimethoprim/nitro

Surgical decompression

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20
Q

What are some pre-renal causes of AKI?

A

40-70%

Renal hypoperfusion (hypovolaemia or sepsis)

Hypotension without hypovolaemia (cirrhosis or septic shock)

Low cardiogenic output (cardiac failure/cardiogenic shock)

Renal hypoperfusion (NSAIDs, ACE-inhibitors)

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21
Q

What are some intrinsic renal causes of AKI?

A

10-50%

Renal parenchyma damage

Acute tubular necrosis (NSAIDs, radiological contrast, uric acid crystals, myeloma)

Vascular

  • renal artery/vein thrombosis
  • cholesterol
  • vasculitis
  • haemolytic uraemic syndrome
  • malignant hypertension

Glomerular- glomerulonephritis, SLE, drugs, infection

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22
Q

What are some post-renal causes of AKI?

A

UTI

Luminal - stones, clots

Mural - malignancy, BPH, strictures

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23
Q

What are risk factors for AKI?

A

> 75

HF

Peripheral vascular disease

Sepsis

Poor fluid intake

CKD

Hypovolaemia

Diabetes

Prostate cancer

Nephrotoxic drugs

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24
Q

How does AKI present?

A

Oliguria

Arrythmias - hyperkalaemia

Uraemia - fatigue, weakness, anorexia, N&V, confusion, seizures and coma

Anaemia and pulmonary oedema - breathlessness

Pericarditis

Impaired platelet function

Postural hypotension

Thirst

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25
Q

How would you investigate AKI?

A

basic metabolic profile - elevated creatinine, high potassium

serum urea to creatinine ratio = 20:1 supports pre-renal

Urinalysis

urine culture

FBC - anaemia, leucocytosis, thrombocytopenia

VBG - met acidosis

fluid challenge - renal function will improve in pre-renal azotaemia

bladder catheterisation

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26
Q

What is a staging system for AKI?

A

KDIGO

based on serum creatinine and urine output

27
Q

How would you treat AKI?

A

Volume expansion and/or red blood cell transfusion - normal saline

Vasopressor - dopamine/adrenaline

Diuretic - furosemide

Renal replacement therapy - haemodialysis for 4-6 hours

Hyperkalaemia - calcium gluconate + insulin and glucose to drive K+ into cells

Acidosis - sodium bicarb

28
Q

What is acute nephritic syndrome characterised by?

A

also known as acute glomerulonephritis

Haematuria - visible or non-visible
Proteinuria (usually <2g in 24 hrs)
Hypertension
Oedema (periorbital, leg or sacral)

29
Q

What are some causes/RFs of acute nephritic syndrome?

A

Often immune response to infection of another disease

IgA nephropathy (most common primary cause)

  • bacterial (MRSA, typhoid, secondary syphilis)
  • Hep B, C
  • Schistomiasis
  • Malaria
  • Post-strep infection 0 classically 2 weeks after tonsilittis
  • Infective endocarditis
  • SLE
  • ANCA assoc. vasculitis
  • Goodpastures
30
Q

What is IgA nephropathy?

A

Commonest cause of nephritic syndrome

Haematuria, IgA deposition in mesangium of kidney

Assoc. with tonsillitis and results in haematuria

31
Q

What is goodpasture’s?

A

co-existence of acute glomerulonephritis and pulmonary alveolar haemorrhage, circulating antibodies directed against an intrinsic antigen to the basement membrane of both kidney and lung

32
Q

How would you investigate acute glomerulonephritis?

A

Urinalysis - haematuria, proteinuria, dysmorphic RBCs, leukocytes and RBC casts

Met profile - creatinine, hypoalbunaemia

LFTs

GFR

FBC - normocytic normochromic anaemia

Lipid profile

USS of kidneys

33
Q

How would you manage acute glomerulonephritis?

A

Phenoxymethylpenicillin

Furosemide

Prednisolone

IF SEVERE - plasmapheresis + corticosteroid + cyclophosphamide

34
Q

What is the classical triad of nephrotic syndrome? What else might you see?

A

Proteinuria - frothy urine

Hypoalbunaemia

Oedema - pitting oedema of ankle, genital , abdo wall and sometimes periorbital

*severe hyperlipidaemia - liver goes into overdrive due to albumin loss and other protein loss which increases risk of blood clots and raised cholesterol

35
Q

What are the causes/RFs of nephrotic syndrome?

A

Structural and functional abnorm of podocytes

Minimal change disease - commonest cause

Membranous nephropathy - penicillamine, gold, NSAIDs, SLE, thyroiditis, Hep B, C, schistomiasis, neoplasia

Focal segmental glomerulosclerosis

Diabetes

Amyloid

Infections

SLE, RA

36
Q

How would you investigate nephrotic syndrome?

A

Renal biopsy - establish cause

urine dip - very high protein

CXR or USS for pleural effusion or ascites

Albumin low

Creatinine, eGFR, lipids and glucose

SLE - ANA, dsDNA, C3, C4

Hep B antigen, Hep C antibody

37
Q

How would you manage nephrotic syndrome?

A

Oedema - furosemide, fluid and salt restriction

Proteinuria - ACEi, ARB

Complications - warfarin, simvastatin

38
Q

What is minimal change disease? What are causes/RFs?

A

Commonest cause of nephrotic syndrome in children - boys under age of 5

characterised by minimal histological changes in the kidney

Idiopathic
Atopy - in 30%
Drugs - NSAIDs, lithium, Abx, Bisphos, Sulfasalazine

Hep C, HIV, TB

39
Q

How would you treat minimal change disease?

A

Corticosteroid - prednisolone

Fluid restriction and low -salt

Albumin and furosemide

40
Q

What is CKD?

A

longstanding, usually progressive, impairment in renal function for more than 3 months

GFR <60mL/min/1.73m2 for more than 3 months with/without evidence of kidney damage

41
Q

Causes/RFs for CKD?

A 
Diabetes
HTN
Atherosclerotic renal vascular disease
PKD
Tuberous sclerosis
IgA nephropathy
SLE
Amyloidosis
Smell and medium-sized vessel vasculitis

Fam Hx CKD

42
Q

Presentation of CKD?

A

Early stages could be asymptomatic

Malaise
Anorexia
Weight loss
Insomnia
Nocturia
Polyuria
itching
N&amp;V and diarrhoea
Amenorrhoea and ED in men
43
Q

What are some complications assoc. with CKD?

A

anaemia - normochromic normocytic anaemia

bone disease - bone pain, osteo-malacia, hyperparathyroidism

neurological - autonomic dysfunction (postural hypotension, disturbed GI motility), peripheral paraesthesiae

CVS - MI, cardiac failure, sudden cardiac death and stroke

Skin disease - pruritus, brown discolouration of nails

44
Q

How would you investigate CKD?

A

ECG - high potassium
Urinalysis - haematuria, proteinuria, MC&S, albumin to creatinine ratio

Biochem - urea, electrolytes, bicarb and creatine, low eGFR, raised ALK phos

Immunology - screen for SLE, scleroderma,and goodpastures

Hep B, C, HIV

USS - renal size

CT - detect stones

45
Q

How is CKD staged?

A

According to GFR

Stage 1 = >90 normal

Stage 2 = 60-89

Stage 3A = 45-59
Stage 3B = 30-44

Stage 4 = 15-29

Stage 5 = <15

46
Q

How would you treat CKD?

A

Stage 1-2 without uraemia

ACE/ARB
Statin
Atenolol
CCB - verapamil

Stage 3-4 without uraemia

ACE/ARB
Statin + ezetimibe
Atenolol
Educate about renal replacement therapy

Stage 5 or with uraemia

Dialysis
Kidney transplant
Sevelamer
Calcimimetic

47
Q

What are the types of renal cystic disease?

A

AD PKD

AR PKD

48
Q

What is the genetics behind PKD?

A

AD

Homozygous - die in womb

mutations in PKD1 (85%) gene in chromosome 16

mutations in PKD2 (15%) gene on chromosome 4

49
Q

How does ADPKD present?

A

clinically silent for years

Symptoms normally 20s onwards

Loin pain
haematuria
loin or abdominal discomfort
nocturia
renal colic
hypertension
renal stones
progressive renal failure
50
Q

What are extra-renal presentation of ADPKD?

A

subarachnoid haemorrhage - berry aneurysm rupture

Polycystic liver disease (70%)

Pancreatitis

Mitral valve prolapse

Ovarian cysts

Diverticular disease

51
Q

How would you investigate ADPKD?

A

Renal USS/CT

<30 y/o - atleast 2 unilateral or bilateral cysts

30-59 y/o - 2 cysts in each kidney

> 60 y/o - 4 cysts in each kidney

urinalysis

serum electrolytes, urea, creatinine

fasting lipid profile

ECG

CT head - check for ruptured intracranial aneurysm

52
Q

Treatment of ADPKD?

A

nothing can slow progression

BP - control ACE-I

Laparoscopic removal of cysts

Serial monitoring of creatinine to track disease progression

53
Q

What mutation for ARPKD?

A

PKHD1 mutation on long arm (q) of chromosome 6

Fam hx

54
Q

What is acute interstitial nephritis? causes?

A

25% of drug-induced acute kidney injury.

penicillin
rifampicin
NSAIDs
allopurinol
furosemide

SLE sarcoidosis

55
Q

How would you investigate acute interstitial nephritis?

A

urea and creatinine

Urine Hansel’s or Wright’s eosinophil stain - eosinophiluria

urinalysis - microhaematuria, sterile pyuria, proteinuria

trial of discontinuing offending medication

ANCA, ANA negative

56
Q

How does acute interstitial nephritis present?

A

fever
rash
oedema

plus AKI and hypertension

57
Q

Differences between IgA nephropathy and post-streptococcal glomerulonephritis?

A

Recent URTI
Haematuria

IgA after 1-2 days and PSG 1-2 weeks after URTI

PSG - proteinuria

58
Q

For renal transplant, how are donors matched?

A

based on human leukocyte antigen

59
Q

What is a typical renal transplant scar? What medications can be given for immunosuppression?

A

Hockey stick incision - hockey stick scar

Tacrolimus
Mycophenolate
Prednisolone

60
Q

What is acute tubular necrosis?

A

damage and death of epithelial cells of the renal tubules - most common cause of AKI

takes 7-21 days to recover

61
Q

What causes acute tubular necrosis? What would be typical on investigations?

A

Shock
Sepsis
Dehydration

Radiology dye
NSAIDs
Heroin

Muddy brown casts on urinalysis is pathognomonic!!

Aso renal tubular epithelial cells in urine

62
Q

What are the different types of renal tubular acidosis?

A

Type 1 - distal tubule pathology (unable to excrete hydrogen ions)

Type 2 - proximal tubule pathology (unable to reabsorb bicarb from urine) Fanconis

Type 3 - combination of type 1 and type 2

Type 4 - reduced aldosterone (adrenal insufficiency, ACE, spironolactone, SLE) - treat with fludrocortisone, sodium bicarb and treat hyperkalaemia

63
Q

Presentation of Rhabdo? Investigations?

A 
Muscle aches and pain
Oedema
Fatigue
Confusion
Red-brown urine

CK - rises until 21 hrs and then remains elevated for 1-3 days

Myoglobinurea - red-brown colour in urine

U&Es

ECG - hyperkalaemia

64
Q

Treatment of Rhabdo?

A

IV fluids

consider sodium bicarb
consider IV mannitol - to increase gfr and reduce oedema

Treat hyperkalaemia

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