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AAClinical school conditions > Mostly renal, some IBS and masses > Flashcards

Mostly renal, some IBS and masses Flashcards

1
Q

Right iliac fossa masses (GI tract)

A

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

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2
Q

Right iliac fossa masses - likely systems involved.

A

GI tract or urogenital.

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3
Q

Right iliac fossa masses (urogenital)

A

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

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4
Q

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

A

Amoebic abscess, actinomycosis, TB mass, pelvic mass.

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5
Q

Abdominal distension causes

A 
The five Fs:
Flatus
Fat
Fluid
Faeces
Fetus
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6
Q

Causes of just ascites (no portal hypertension)

A 
Malignancy
Pancreatitus
Low albumin
Myxodema (hypothyroidism)
CCF pericarditis
Infections like TB.
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7
Q

Causes of ascites with portal hypertension.

A

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

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8
Q

Left upper quadrant masses - probable organs affected

A

Spleen, stomach, kidney, colon, pancreas

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9
Q

Faeculent vomit

A

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

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10
Q

With abdominal pain check

A

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

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11
Q

Causes of right hypochondrial pain

A

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

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12
Q

Acute pancreatitis definition

A

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

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13
Q

Acute pancreatitis: presenting symptoms

A

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

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14
Q

Acute pancreatitis: non-presenting symptoms.

A

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

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15
Q

Acute pancreatitis: investigations.

A

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

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16
Q

Acute pancreatitis predisposing factors.

A

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

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17
Q

Odynophagia

A

Pain on swallowing, commonly due to mouth ulcers

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18
Q

How to identify heartburn as non-cardiac

A

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

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19
Q

Deep and poorly localised midline pain is caused by…

A

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

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20
Q

Epigastric pain arises from

A

Stomach, liver, spleen and biliary system

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21
Q

Umbilical pain arises from

A

Small bowl and appendix.

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22
Q

Suprapubic pain arises from

A

The colon, although this can be localised.

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23
Q

Midline pain radiating to the back

A

Likely to be pancreatic

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24
Q

Main parts of kidney

A

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

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25
Q

Layers of tissue around kidney

A

Perinephric fat, renal fascia, paranephric fat.

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26
Q

Anatomy of left renal vein

A

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

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27
Q

Constrictions of the ureter

A

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

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28
Q

Urinary tract stones - age, sex and predisposition

A

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

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29
Q

What is a urinary tract stone.

A

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

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30
Q

Urinary tract imaging

A

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

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31
Q

Types of renal tumours

A 
More common: renal cell carcinoma (can have venous extension) - 90%. 
Less common (5%): transitional cell tumours.
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32
Q

Common renal diagnostic tests

A

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

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33
Q

Symptoms and causes of acute renal failure

A

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

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34
Q

Pre-renal causes of acute kidney failure.

A

Hypotension, volume depletion, sepsis and renovascular disease.

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35
Q

Symptoms of chronic kidney disease.

A

Increased urea and creatinine, increased phosphate and decreased haemoglobin.

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36
Q

Common causes of chronic kidney disease

A

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

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37
Q

Complications of nephrotic syndrome

A

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

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38
Q

Symptoms of nephritic syndrome

A

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

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39
Q

Nephrotic syndrome - symptoms and most common cause.

A

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

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40
Q

Effects of treatment of membranous glomerulonephritis.

A

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

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41
Q

Pre-renal causes of kidney failure

A

Rapid drop in blood pressure.

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42
Q

Renal causes of kidney failure.

A

Increase in blood pressure, diabetes.

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43
Q

Post-renal causes of kidney failure

A

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

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44
Q

The functional unit of the kidney

A

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

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45
Q

Normal urine output

A

About 0.5 ml/kg/hr

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46
Q

Position of kidney

A

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

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47
Q

Parts of the nephron

A

The corpuscle and the tubule

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48
Q

Parts of the renal corpuscle

A

Glomerulus (with 3 membranes)

Bowman’s capsule.

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49
Q

Parts of the renal tubule

A

Proximal tubule
Loop of Henle
Distal tubule
Collecting duct

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50
Q

Parts of the Loop of Henle (in kidney)

A

Thin descending limb
Thin ascending limb
Thick ascending limb.

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51
Q

Role of distal tubule in kidney

A

Hormone sensitive water balance.

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52
Q

Parts of the juxta-glomerular apparatus

A

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

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53
Q

Stimulation and effect of renin

A

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).

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54
Q

Stimulation of erythropoietin secretion

A

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

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55
Q

Role of ADH

A

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.

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56
Q

IBS def

A

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

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57
Q

IBS epidemiology

A

10-20% of population of UK. More common in women.

Peak prevalence between ages of 20-30.

58
Q

IBS aetiology

A

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

59
Q

IBS clinical presentation

A 
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
Q

IBS investigations

A

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

61
Q

IBS management

A

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

Placebo effect strong

62
Q

Clinical features of peptic ulcer disease

A

Epigastric pain, bloating, fullness, heartburn.

63
Q

Clinical features of peptic ulcer disease - duodenal ulcers

A

Epigastric pain before meals or at night, relieved by milk

bloating, fullness, heartburn.

64
Q

ALARM Signs for peptic ulcer disease

A 
Anaemia
Loss of weight
Anorexia
Recent onset/progressive course
Melaena/haemoptysis
Swallowing difficulties.
65
Q

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

A

Test for H. pylori

66
Q

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

A

Endoscopy

67
Q

Treatment of peptic ulcer disease

A

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

68
Q

Complications of peptic ulcer disease

A

Bleeding, perforation, malignancy

69
Q

Tenesmus

A

A feeling of incomplete emptying after defecation

70
Q

Questions to ask about diarrhoea

A 
Acute or chronic? Watery?
Blood?
Mucus?
Frank pus?
Explosive?
Pain?
71
Q

Causes of diarrhoea with blood

A

Infections
Amoebiasis
UC, Crohn’s, cancer
Various colitides

72
Q

Causes of diarrhoea with mucus

A

IBS, cancer, polyps

73
Q

Causes of diarrhoea with frank pus

A

IBD, diverticulitis, fistula

74
Q

Causes of explosive diarrhoea

A

Mostly infections

75
Q

Management of acute abdomen

A

Take basic obs to triage
History
Analgesia
Investigate

76
Q

Basic investigations for acute abdomen

A

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

77
Q

Urolithiasis - epidemiology, hereditary factors, acquired factors.

A

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
Q

Types of urinary tract stones

A

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

79
Q

Features of calcium oxalate kidney stones

A

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

80
Q

Features of struvite stones

A

Usually in proteus or staphylococci infection.

81
Q

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

A

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
Q

Conditions causing high conc of metabolic products in glomerular filtrate

A

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
Q

What values define hypercalciuria?

A

In men more than 7.5 mmols/day

In women more than 6.2 mmols/day.

84
Q

What is hyperoxaluria a risk factor

A

It causes formation of calcium oxalates without hypercalciuria.

85
Q

What causes hyperoxaluria

A

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

86
Q

Conditions predisposing to stone formation (4)

A

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

87
Q

What causes changes to urine pH

A

Diet and infection. Affects preciptation of salts.

88
Q

What causes urinary stagnation

A

Obstruction of urinary flow

89
Q

What are stone forming inhibitors in the urine?

A

Citrate, pyrophosphate and glycoproteins

90
Q

What is acute pyelonephritis?

A

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

91
Q

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

A

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

92
Q

What are complication of acute pyelonephritis?

A

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

93
Q

Causes of acute pyelonephritis - acronym

A

POST CARDS

94
Q

Causes of acute pyelonephritis - POST CARDS

A 
Pyelonephritis
Obstruction of urogenital tract
Sickle cell disease
Tuberculosis
Chronic liver disease
Analgesia or alcohol abuse
Renal transplant rejection
Diabetes mellitus
Systemic vasculitis.
95
Q

How do you treat acute pyelonephritis?

A

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

96
Q

Epidemiology for cholelithiasis

A

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

97
Q

Risk factors for cholestrol stones

A 
Age
Female sex hormones
Obesity
Rapid weight loss
Genetic abnormalities
Hyperlipidaemia
98
Q

Risk factors for pigment stones

A

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

99
Q

Imaging for gallstones

A

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
Q

Pathogenesis of gallstones

A 
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
Q

Acute tubular necrosis - causes

A

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

102
Q

Systemic diseases causing glomerular lesions - classes

A

Immune complex mediated
Metabolic
Vasculitis

103
Q

Immune complex mediated causes of glomerular lesions

A

SLE
Henoch-Schonlein
Bacterial endocarditis
Goodpasture’s

104
Q

SLE damage to kidneys and treatment

A

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

105
Q

What is Henoch-Schonlein purpura?

A

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

106
Q

What effects can bacterial endocarditis have on the kidneys?

A

Antibody deposition and emboli can cause infarction

107
Q

What are the antibodies against in Goodpasture’s syndrome?

A

Anti-basement membrane antibodies - affects lungs and kidneys.

108
Q

What are metabolic causes of glomerular damage?

A

Diabetic glomerulosclerosis.

109
Q

Which vasculitides commonly cause glomerular damage?

A

Microscopic polyarteritis nodosa (necrotising)

Wegener’s (rare, necrotising, affects U and L resp tract and kidneys)

110
Q

Causes of damage to tubules and calyces

A

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

111
Q

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

A

T-cell mediated inflamation

112
Q

What causes urate nephropathy?

A

Increased synthesis in psoriasis or malignancy

Decreased clearance in CRF (which can lead to gout)

113
Q

How does hypercalcaemia lead to tubule damage?

A

By accumulating calcium in the cells and by stone formation.

114
Q

How does multiple myeloma cause kidney damage?

A

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

115
Q

What are the hereditary glomerular diseases?

A

Alport’s and Fabry’s

116
Q

What is Alport’s disease?

A

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

117
Q

What is Fabry’s disease?

A

A glycolipid disorder leading to cardiac issue and glomerulonephritis.

118
Q

Infective causes of glomerulonephritides.

A

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

119
Q

Results of infective GN

A

proteinuria, haematuria, low GFR

120
Q

Type of GN caused commonly by infection

A

Diffuse and proliferative.

121
Q

What is vesico-ureteric reflux associated with?

A

Reflux nephropathy

122
Q

What is the result of reflux nephropathy?

A

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

123
Q

What are the common benign causes of kidney tumours?

A

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

124
Q

Renal cell carcinoma presentation

A

Haematuria, paraneoplastic syndromes

125
Q

Renal cell carcinoma common paraneoplastic syndromes

A

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

126
Q

Spread of renal cell carcinoma

A

Via direct invasion, via lymph to lumbar nodes,

127
Q

Treatment of renal cell carcinoma

A

Nephrectomy with radiotherapy.

128
Q

Common kidney malignancy in children

A

Wilm’s tumour.

129
Q

Where do the kidney lymph nodes drain?

A

To the para-aortic lymph nodes.

130
Q

Polycystic disease definition

A

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

131
Q

When and how does polycystic disease present?

A

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

132
Q

What is polycystic kidney disease associated with?

A

SAH or cerebral haemorrhage.

133
Q

How does htn affect renal vessels?

A

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

134
Q

What effect does accelerated htn have on the kidney?

A

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

135
Q

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

A

HUS and TTP.

Haemolysis, thrombocytopenia, ARF.

136
Q

Histologically what kind glomerulonephritis is acute post-infective GN?

A

All cells involved, so diffuse proliferative.

137
Q

What causes rapidly progressive GN?

A

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

138
Q

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

A

Children.

139
Q

What are the common causes of membranous GN?

A

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

140
Q

What are the types of membranoproliferative GN?

A

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

141
Q

What are the causes of focal segmental glomerulosclerosis?

A

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

142
Q

IgA nephropathy presentations

A

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

AAClinical school conditions (32 decks)

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