Mostly renal, some IBS and masses Flashcards Preview

► Med Misc 46 > Mostly renal, some IBS and masses > Flashcards

Flashcards in Mostly renal, some IBS and masses Deck (142):
1

Right iliac fossa masses (GI tract)

Appendix mass/abscess, Intussusception, caecal carcinoma, Crohn's disease.

2

Right iliac fossa masses - likely systems involved.

GI tract or urogenital.

3

Right iliac fossa masses (urogenital)

Transplanted kidneys, kidney malformation, tumour in an undescended testis.

4

Right iliac fossa masses (random, not GI or urogenital)

Amoebic abscess, actinomycosis, TB mass, pelvic mass.

5

Abdominal distension causes

The five Fs:
Flatus
Fat
Fluid
Faeces
Fetus

6

Causes of just ascites (no portal hypertension)

Malignancy
Pancreatitus
Low albumin
Myxodema (hypothyroidism)
CCF pericarditis
Infections like TB.

7

Causes of ascites with portal hypertension.

Cirrhosis, portal nodes, Budd-Chiari syndrome, IVC or portal vein thrombosis.

8

Left upper quadrant masses - probable organs affected

Spleen, stomach, kidney, colon, pancreas

9

Faeculent vomit

Suggests low intestinal obstruction or the presence of a gastrocolic fistula.

10

With abdominal pain check

1) Site, intensity, character, duration and frequency.
2) Aggravating and relieving factors.
3) Any associated symptoms.

11

Causes of right hypochondrial pain

Gall bladder or biliary tract. More rarely can be hepatic congestion or peptic ulcer disease.

12

Acute pancreatitis definition

Inflammation of the pancreatic gland initiated by acute injury on a background of a previously normal pancreas.

13

Acute pancreatitis: presenting symptoms

Epigastric pain accompanied by nausea and vomiting, with involvement of retroperitoneum leading to back pain.

14

Acute pancreatitis: non-presenting symptoms.

Widespread tenderness in abdomen with guarding. Reduced or absent bowel sounds.

15

Acute pancreatitis: investigations.

Blood tests showing raised serum and/or raised urinary amylase.

16

Acute pancreatitis predisposing factors.

Alcoholism (more in men), gallstones (more in women).

17

Odynophagia

Pain on swallowing, commonly due to mouth ulcers

18

How to identify heartburn as non-cardiac

Burning sensation, not crushing, upwards radiation, occurs on lying down or bending forward.

19

Deep and poorly localised midline pain is caused by...

Distension of hollow organs, mesenteric traction or excessive smooth muscle contraction. Pain is conducted by sympathetic splanchnic nerves.

20

Epigastric pain arises from

Stomach, liver, spleen and biliary system

21

Umbilical pain arises from

Small bowl and appendix.

22

Suprapubic pain arises from

The colon, although this can be localised.

23

Midline pain radiating to the back

Likely to be pancreatic

24

Main parts of kidney

hilum, renal cortex, renal medulla. Pyramids and columns.

25

Layers of tissue around kidney

Perinephric fat, renal fascia, paranephric fat.

26

Anatomy of left renal vein

It passes between the abdominal aorta and the superior mesenteric artery, and can be compressed by an aneurysm in either.

27

Constrictions of the ureter

ureteropelvic junction,
crossing the common iliac vessels,
entering the bladder

28

Urinary tract stones - age, sex and predisposition

More men than women, tends to be in 20-60 yr olds, a sedentary lifestyle is predisposing.

29

What is a urinary tract stone.

A polycrystalline aggregate of precipitated soluble salts in the urinary tract.

30

Urinary tract imaging

Abdominal X-ray can show stones.
US scanning (for dilatations)
IV urogram
CT.

31

Types of renal tumours

More common: renal cell carcinoma (can have venous extension) - 90%.
Less common (5%): transitional cell tumours.

32

Common renal diagnostic tests

Clearance tests
Concentration and dilution tests
Serum creatinine and BUN
Protein in urine

33

Symptoms and causes of acute renal failure

Symptoms: elevated serum creatinine. Renal function declined over days to weeks.
Causes: pre-renal > renal > post renal.

34

Pre-renal causes of acute kidney failure.

Hypotension, volume depletion, sepsis and renovascular disease.

35

Symptoms of chronic kidney disease.

Increased urea and creatinine, increased phosphate and decreased haemoglobin.

36

Common causes of chronic kidney disease

Diabetes mellitus, hypertensive nephropathy, obstructive uropathy, chronic primary glomerulonephritis.

37

Complications of nephrotic syndrome

Loss of proteins leads to increased risk of infection and thromboembolism. Also have hypercholestraemia.

38

Symptoms of nephritic syndrome

Hypertension, haematuria and acute renal failure (oliguria).
Also fluid retention, uraemia, and proteinuria.

39

Nephrotic syndrome - symptoms and most common cause.

Symptoms: proteinuria of at least 3g/24hr, hypoalbuminaemia, oedema. Hypercholesteraemia.
Most common cause is membranous glomerulonephritis.

40

Effects of treatment of membranous glomerulonephritis.

1/3 recover with conservative treatment, 1/3 don't, and 1/3 get worse.

41

Pre-renal causes of kidney failure

Rapid drop in blood pressure.

42

Renal causes of kidney failure.

Increase in blood pressure, diabetes.

43

Post-renal causes of kidney failure

Obstruction (stones or malignancy).
Retroperitoneal fibrosis.
Malignancy outside urinary tract causing pressure and obstruction.

44

The functional unit of the kidney

The nephron. There are roughly 10 to the 6 in each kidney.

45

Normal urine output

About 0.5 ml/kg/hr

46

Position of kidney

10-12 cm long between T12 and L3. Right kidney is lower.

47

Parts of the nephron

The corpuscle and the tubule

48

Parts of the renal corpuscle

Glomerulus (with 3 membranes)
Bowman's capsule.

49

Parts of the renal tubule

Proximal tubule
Loop of Henle
Distal tubule
Collecting duct

50

Parts of the Loop of Henle (in kidney)

Thin descending limb
Thin ascending limb
Thick ascending limb.

51

Role of distal tubule in kidney

Hormone sensitive water balance.

52

Parts of the juxta-glomerular apparatus

Granular cells secreting renin, the macula densa alter GFR and renin secretion.

53

Stimulation and effect of renin

Decrease in Na+ filtered, or decrease in afferent arteriole pressure or sympathetic B receptor stimulation all lead to renin secretion.
Renin catalyses conversion of angiotensinogen to angiotensin I (which is converted to angiotensin II, a vasoconstrictor).

54

Stimulation of erythropoietin secretion

Hypoxia of the inner cortex and peritubular interstitium and polycystic kidney disease increase production.
Chronic renal failure decreases production.

55

Role of ADH

Short acting increase in water reabsorption in the distal tubule and collecting duct. Decreased ADH leads to diabetes insipidus. Increased can be due to a pituitary tumour.

56

IBS def

A relapsing functional bowel disorder in which abdominal pain or discomfort is associated with defecation or a change in bowel habit.

57

IBS epidemiology

10-20% of population of UK. More common in women.
Peak prevalence between ages of 20-30.

58

IBS aetiology

Seems to involve abnormal smooth muscle activity, visceral hypersensitivity and abnormal central pain processing.

59

IBS clinical presentation

Pain or discomfort.
1/3 have constipation
1/3 have diarrhoea
1/3 have both hard and soft stools.
Chronic with remissions. Urgent morning rush common.

60

IBS investigations

Bloods
Coeliac screen
CA-125 for women at risk of ovarian cancer
Faecal calprotectin for those who could have IBD.

61

IBS management

Diet (limit/increase high-fibre) + fluids.
Placebo effect strong

62

Clinical features of peptic ulcer disease

Epigastric pain, bloating, fullness, heartburn.

63

Clinical features of peptic ulcer disease - duodenal ulcers

Epigastric pain before meals or at night, relieved by milk
bloating, fullness, heartburn.

64

ALARM Signs for peptic ulcer disease

Anaemia
Loss of weight
Anorexia
Recent onset/progressive course
Melaena/haemoptysis
Swallowing difficulties.

65

With a patient with peptic ulcer disease, who is under 55 yr, what investigation do you do?

Test for H. pylori

66

With a patient with peptic ulcer disease, new onset over 55yr or with ALARM Signs, what investigation do you do?

Endoscopy

67

Treatment of peptic ulcer disease

Lifestyle modifications
H. pylori triple therapy
PPIs (or H2 blockers, sometimes)
Stop drugs causing ulcers.

68

Complications of peptic ulcer disease

Bleeding, perforation, malignancy

69

Tenesmus

A feeling of incomplete emptying after defecation

70

Questions to ask about diarrhoea

Acute or chronic? Watery?
Blood?
Mucus?
Frank pus?
Explosive?
Pain?

71

Causes of diarrhoea with blood

Infections
Amoebiasis
UC, Crohn's, cancer
Various colitides

72

Causes of diarrhoea with mucus

IBS, cancer, polyps

73

Causes of diarrhoea with frank pus

IBD, diverticulitis, fistula

74

Causes of explosive diarrhoea

Mostly infections

75

Management of acute abdomen

Take basic obs to triage
History
Analgesia
Investigate

76

Basic investigations for acute abdomen

Bloods - FBC, U&Es, CRP.
MSU and blood cultures
Stool tests, plain radiology, special tests.

77

Urolithiasis - epidemiology, hereditary factors, acquired factors.

5-10% of population. More men than women.

Hereditary factors include cystinuria, primary hyperoxaluria

Acquired factors include hypercalcaemia, hypercalciuria, sarcoidosis, gout and leukaemia.

4 types of stone

78

Types of urinary tract stones

70% calcium oxalate/phosphate
15% struvite stones
5-10% uric acid
1-5% cysteine.

79

Features of calcium oxalate kidney stones

White, hard, radiopaque. Calcium phosphate often causes staghorn in renal pelvis, calcium oxalate is generally present in the ureter.

80

Features of struvite stones

Usually in proteus or staphylococci infection.

81

How do you identify what type of kidney stone the patient has?

Either analyse stone, or do
Serum calcium and uric acid analysis
Urnialysis (volume, calcium, oxalates and cysteine levels)
Urine pH – more than 8 means probably UTI.

82

Conditions causing high conc of metabolic products in glomerular filtrate

Low urinary volume due to fluid restriction (increase fluids).
Increased fluid loss.
Increased excretion of metabolic products forming stones.
High plasma volume leading to high filtrate level.
Low tubular reabsorption from the filtrate.

83

What values define hypercalciuria?

In men more than 7.5 mmols/day
In women more than 6.2 mmols/day.

84

What is hyperoxaluria a risk factor

It causes formation of calcium oxalates without hypercalciuria.

85

What causes hyperoxaluria

Diet rich in oxalates (restrict diet) or increase absorption in fat malabsorption. Or can be primary.

86

Conditions predisposing to stone formation (4)

High conc of metabolic products in glomerular filtrate
Changes in urine pH
Urinary stagnation
Deficiency of stone forming inhibitors in urine.

87

What causes changes to urine pH

Diet and infection. Affects preciptation of salts.

88

What causes urinary stagnation

Obstruction of urinary flow

89

What are stone forming inhibitors in the urine?

Citrate, pyrophosphate and glycoproteins

90

What is acute pyelonephritis?

Suppurative inflammation of the kidney, commonly caused by E. Coli

91

What parts of the kidney are involved in acute pyelonephritis and how?

Neutrophils within the tubules and interstitium, glomeruli only involved in severe candida disease.
Yellow white cortical abscesses with surrounding hyperaemia.

92

What are complication of acute pyelonephritis?

scarring. Complications include pyonephritis, when the pelvis, calyces and ureter fill with pus, peri-nephric abscess and papillary necrosis.

93

Causes of acute pyelonephritis - acronym

POST CARDS

94

Causes of acute pyelonephritis - POST CARDS

Pyelonephritis
Obstruction of urogenital tract
Sickle cell disease
Tuberculosis
Chronic liver disease
Analgesia or alcohol abuse
Renal transplant rejection
Diabetes mellitus
Systemic vasculitis.

95

How do you treat acute pyelonephritis?

Commonly caused by E. Coli, s while awaiting blood cultures, treat with ciprofloxacin for 7 days.

96

Epidemiology for cholelithiasis

Gallstones. 10-20% of adult populations, with higher prevalence in some Native American tribes. Pigment stones common in non-Western populations.

97

Risk factors for cholestrol stones

Age
Female sex hormones
Obesity
Rapid weight loss
Genetic abnormalities
Hyperlipidaemia

98

Risk factors for pigment stones

Chronic haemolytic syndromes,
Biliary infection
Ileal disease
Cystic fibrosis with pancreatic insufficiency.

99

Imaging for gallstones

If no symptoms, or simply pain, then use US.
If worried about pancreatitis or peritonitis then use CT
Use MRCP if suspected biliary duct stone.

100

Pathogenesis of gallstones

An imbalance in bile composition rendering the chloesterol and calcium salts insoluble - this can be caused by cholesterol supersaturation in bile (hepatic cholesterol hypersecretion), crystal nucleation (mucin hypersecretion aids this),
stone growth (gall bladder hypermobility)

101

Acute tubular necrosis - causes

Ischaemic (hypotension, hypovolaemia, NSAIDs potentiate ischaemia by inhibiting prostaglandins)
Toxic (nephrotoxic drugs)

102

Systemic diseases causing glomerular lesions - classes

Immune complex mediated
Metabolic
Vasculitis

103

Immune complex mediated causes of glomerular lesions

SLE
Henoch-Schonlein
Bacterial endocarditis
Goodpasture's

104

SLE damage to kidneys and treatment

Minimal change to diffuse proliferative GN
Immune complex deposition leads to basement membrane and endothelial thickening.
Treat with immunosuppression

105

What is Henoch-Schonlein purpura?

A immune mediated vasculitis mainly in kids affecting the skin (purpuric rash), joints (pain), intestine (pain, vomiting) and kidneys (GN)

106

What effects can bacterial endocarditis have on the kidneys?

Antibody deposition and emboli can cause infarction

107

What are the antibodies against in Goodpasture's syndrome?

Anti-basement membrane antibodies - affects lungs and kidneys.

108

What are metabolic causes of glomerular damage?

Diabetic glomerulosclerosis.

109

Which vasculitides commonly cause glomerular damage?

Microscopic polyarteritis nodosa (necrotising)
Wegener's (rare, necrotising, affects U and L resp tract and kidneys)

110

Causes of damage to tubules and calyces

Infection, some drugs (NSAIDs, penecillin, rifampicin), urate nephropathy, chronic hypercalcaemia, multiple myeloma.

111

How what mediates the damage to the tubules and calyces causes by certain drugs (penecillin, rifampicin)

T-cell mediated inflamation

112

What causes urate nephropathy?

Increased synthesis in psoriasis or malignancy
Decreased clearance in CRF (which can lead to gout)

113

How does hypercalcaemia lead to tubule damage?

By accumulating calcium in the cells and by stone formation.

114

How does multiple myeloma cause kidney damage?

By Bence-Jones proteins whose light chains lead to inflammation,
Paraproteins,
Urate deposition,
Hypercalcaemia.

115

What are the hereditary glomerular diseases?

Alport's and Fabry's

116

What is Alport's disease?

An X-linked collagen abnormality causing glomerulonephritis, ocular abnormalities and hearing loss.

117

What is Fabry's disease?

A glycolipid disorder leading to cardiac issue and glomerulonephritis.

118

Infective causes of glomerulonephritides.

Post-streptococcal (after tonsil, pharynx or skin infection) or non-strep.

119

Results of infective GN

proteinuria, haematuria, low GFR

120

Type of GN caused commonly by infection

Diffuse and proliferative.

121

What is vesico-ureteric reflux associated with?

Reflux nephropathy

122

What is the result of reflux nephropathy?

Increased ureteric pressure leads to scarring, deformation and dilated calyces, and formation of eosinophilic casts.

123

What are the common benign causes of kidney tumours?

Renal fibroma and cortical adenoma - which looks like RCC histologically.

124

Renal cell carcinoma presentation

Haematuria, paraneoplastic syndromes

125

Renal cell carcinoma common paraneoplastic syndromes

PTH leads to hypercalcaemia
ACTH leads to Cushing's syndrome
EPO leads to polycythaemia
Renin leads to htn.

126

Spread of renal cell carcinoma

Via direct invasion, via lymph to lumbar nodes,

127

Treatment of renal cell carcinoma

Nephrectomy with radiotherapy.

128

Common kidney malignancy in children

Wilm's tumour.

129

Where do the kidney lymph nodes drain?

To the para-aortic lymph nodes.

130

Polycystic disease definition

Autosomal dominant condition involving PKD1, 2 or 3, leading to the formation of of multiple cysts and impairment of renal function.

131

When and how does polycystic disease present?

In the 30-40s wiht htn, loin pain, haematura and large palpable kidneys.
Kidney failure 40-60s.

132

What is polycystic kidney disease associated with?

SAH or cerebral haemorrhage.

133

How does htn affect renal vessels?

Leads to hyperplasia and hyalinisation of the arteriole wall called benign nephrosclerosis and hence ischaemic atrophy of the nephrons.

134

What effect does accelerated htn have on the kidney?

It causes petechial haemorrhages and fibrin deposits (leading to fibrinoid necrosis) which lead to severe arterial damage, proteinuria, haematuria and renal failure.

135

What are the thrombotic microangiopathies leading to renal damage? And what is the triad of symptoms they cause?

HUS and TTP.
Haemolysis, thrombocytopenia, ARF.

136

Histologically what kind glomerulonephritis is acute post-infective GN?

All cells involved, so diffuse proliferative.

137

What causes rapidly progressive GN?

SLE, Wegener's granulomatosis and microscopic polyangiitis - epithelial cell proliferate causing cresent formation.

138

Which group of patients are mostly likely to have minimal change GN?

Children.

139

What are the common causes of membranous GN?

Subepithelial immune complex deposition and basement membrane tumours. Usually idiopathic.

140

What are the types of membranoproliferative GN?

Usually primary causes. Type 1 is due to immune complexes, type 2 due to complement.

141

What are the causes of focal segmental glomerulosclerosis?

Heroin use, AIDS, reaction to chronic proteinuria, idiopathic.

142

IgA nephropathy presentations

young male, recurrent episodes of macroscopic haematuria
typically associated with mucosal infections e.g., URTI
nephrotic range proteinuria is rare
renal failure