SBA revision 2 Flashcards

1
Q

lower urinary tract symptoms (LUTS)

A

storage (aka irritative) and voiding (aka obstructive)
symptoms and remembered using the mnemonic FUN (storage) WISE
(voiding): Frequency, Urgency, Nocturia, Weak stream, Intermittency,
Straining, incomplete Emptying.

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2
Q

`Tumor markers

A

CA 15-3 = Breast cancer
CA 19-9 = Pancreatic cancer
CA 125 = Ovarian cancer
CEA = Colorectal cancer
aFP = Liver cancer, Testicular cancer (non-seminomas)
b-hCG = Choriocarcinoma, Germ cell tumours
S100 = Melanoma
Calcitonin = Medullary thyroid cancer
PSA = Prostate cancer
Thyroglobulin = Thyroid cancer (used post-thyroidectomy to monitor
completeness of removal)

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3
Q

Breathing patterns

A

Kussmaul breathing is characterised by deep, sighing breaths. It is a
compensatory response to severe metabolic acidosis (e.g. ketoacidosis) —
the deep breaths help to blow off carbon dioxide and raise pH.
Cheyne–Stokes breathing is a cyclic breathing pattern in which breathing
gets progressively deeper, then progressively shallower followed by a
period of apnoea. Causes include brainstem damage or herniation.
Hypoventilation broadly refers to a decrease in ventilation. Biot’s respi
ration is characterised by clusters of rapid, shallow inspirations and
expirations interspersed amongst periods of apnoea. It is also caused by
brainstem damage. Apnoea refers to the temporary cessation of breathing.

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4
Q

Tumors and nodes

A

Testicular tumours -spread to the para-aortic lymph nodes
Scrotal and penile tumours and
infections -will lead to enlargement of inguinal lymph nodes

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5
Q

HF CXR

A

ABCDE: Alveolar shadowing, Kerley B lines,

Cardiomegaly, Dilated upper lobe vessels, Effusion

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6
Q

Stroke management

A

There are two main types of stroke: ischaemic (80%) — in
which the brain is temporarily starved of blood due to thrombosis, emboli
or hypotension — and haemorrhagic — where a bleed within the brain
creates pressure that damages the brain tissue. Such bleeds may come from
microaneurysm rupture, trauma, tumours, vasculitis or arteriovenous
malformations. The single most important risk factor is hypertension, but
others include smoking, hyperlipidaemia and diabetes. Management of
ischaemic and haemorrhagic strokes differ, so an urgent CT head scan is
required to distinguish between the two. Once a bleed has been excluded
(by the absence of bleeding on a CT head scan), you need to determine the
next stage of the management by considering the time since the onset of
symptoms. If the onset of symptoms was less than 4.5 hours ago, the patient
should be thrombolysed with alteplase and given aspirin within 24 hrs. If
the onset of symptoms was more than 4.5 hrs ago, the patient should be
given antiplatelet therapy and undergo a swallow assessment and GCS
monitoring.

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7
Q

Antibody markers

A

pANCA - Primary sclerosing cholangitis,microscopic
polyangiitis, granulomatosis with polyangiitis and rheumatoid arthritis
AMA - primary biliary cirrhosis (PBC).
ASLA - type 1 autoimmune hepatitis
ALKM-1 - and type 2 autoimmune hepatitis

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8
Q

Causes of dysphagia

A
• Obstructive
• Oesophageal carcinoma
• Peptic strictures (D)
• Oesophageal web/ring (B)
• Gastric carcinoma
• Pharyngeal carcinoma (A)
• Extrinsic pressure from, for example, lung carcinoma, retrosternal
goitre (C)
• Oesophageal motility disorders
• Achalasia (E)
• Systemic sclerosis
• Stroke
• Myasthenia gravis
• Neurological degenerative conditions, e.g. motor neurone disease,
Parkinson’s disease
• Others
• Oesophagitis
• Pharyngeal pouch
• Oesophageal candidiasis
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9
Q

Budd -Chiari triad
hepatic
vein outflow obstruction

A

Abdo pain, hepatomegaly, ascites

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10
Q

Causes of Hepatomegaly

A

The causes of hepatomegaly can be classified according to:
1 Maligancy: primary (e.g. HCC) or secondary.
2 Hepatic congestion secondary to: right heart failure, Budd–Chiari
syndrome.
3 Infection: hepatitis (secondary to viruses, malaria, shistosomiasis,
amoebic abscess, hydatid cyst), infectious mononucleosis.
4 Haematological: leukaemia, lymphoma, myeloproliferative disorders,
such as myelofibrosis, sickle-cell disease, haemolytic anaemias.
5 Anatomical: Riedel’s lobe.
6 Other causes include early cirrhosis, fatty liver, porphyria,
amyloidosis, Gaucher’s disease.

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11
Q

drug induced cholestasis

A
  • Clavulanic acid
  • Penicillins
  • Oestrogens
  • Erythromycin
  • Chlorpromazine
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12
Q

Causes of finger clubbing

A
Inflammatory bowel disease
 liver
cirrhosis, 
primary biliary cirrhosis, oesophageal leiyomyoma, coeliac
disease and achalasia
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13
Q

Causes of upper gastrointestinal bleeding

A
  • peptic ulcers – approximately 35–50 per cent of bleeds (B);
  • Mallory–Weis tears – 15 per cent (A);
  • oesophagitis – 5–15 per cent;
  • gastritis and gastric erosions – 5–15 per cent;
  • oesophageal varices – 5–10 per cent (C);
  • drugs (e.g. NSAIDs, steroids, anticoagulants) – 5 per cent (D);
  • upper GI malignancy – 5 per cent (E);
  • rarer causes (<5 per cent):
  • Dieulafoy’s lesion;
  • angiodysplasia;
  • haemobilia;
  • aorto-enteric fistula
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14
Q

causes of portal hypertension (>10 mmHg)

A

1) Pre-hepatic: portal-vein thrombosis, splenic vein
thrombosis; (2) Hepatic: cirrhosis (accounts for 80 per cent of causes of
portal hypertension), shistosomiasis (most common cause worldwide),
sarcoidosis, myeloproliferative disease, congenital hepatic fibrosis; and
(3) Post-hepatic: Budd–Chiari syndrome, right heart failure, constrictive
pericarditis, veno-occlusive disease

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15
Q

Prophylaxis for the prevention of variceal

bleeding portal hypertension (>12 mmHg)

A

(1) Primary: non-selective β-blockade (e.g.
propranolol) and/or endoscopic banding ligation; (2) Secondary (i.e. after
an initial variceal bleed: non-selective β-blockade, endoscopic banding
ligation, transjugular intrahepatic portosystemic shunting (TIPPS)

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16
Q

causes of liver cirrhosis

A

•chronic alcoholism
• non-alcholic steatohepatitis,
•chronic hepatitis B and C infections
•autoimmune conditions (e.g. autoimmune hepatitis, primary biliary cirrhosis, primary sclerosing cholangitis),
•genetic disorders (e.g. haemachromatosis, Wilson’s disease), cryptogenic (in
approximately 20 per cent), Budd–Chiari syndrome

17
Q

signs of chronic liver disease

A

leuconychia, clubbing,
palmer erythema, hyperdynamic circulation, Dupuytren’s contracture, spider
naevi, xanthelasma, gynaecomastia, atrophic testes, loss of body hair,
hepatomegaly (occurs in initial stages then shrinks in late disease).

18
Q

Complications of liver cirrhosis

A

(1) Hepatic failure leading to
conditions such as coagulopathy, encephalopathy, hypoalbuminaemia,
sepsis and hypoglycaemia; (2) Portal hypertension leading to ascites,
splenomegaly, oesophageal varices and other portosystemic shunts;
(3) Increased risk of hepatocellular carcinoma.

19
Q

Macrocytosis, i.e. an elevated MCV (>96 fL)

A

megaloblastic anaemia secondary to vitamin B12 and folic acid
deficiency;
• chronic alcoholism and/or alcoholic liver disease (most common
causes of all causes of macrocytosis), pregnancy, hypothyroidism,
reticulocytosis, aplastic anaemia, myelodysplastic syndromes and can
also be caused by drugs that inhibit DNA synthesis (e.g. azathioprine);

20
Q

primary biliary cirrhosis SIGNS

A

jaundice, xanthelasma, xanthomata, skin pigmentation,

splenomegaly and hepatomegaly

21
Q

Ascites occur secondary to

A

conditions leading to venous hypertension (e.g. cirrhosis, congestive
heart failure, constrictive pericarditis, Budd–Chiari syndrome, portal
vein thrombosis);
• hypoalbuminaemia (e.g. nephrotic syndrome, malnutrition);
• malignant disease (e.g. secondary metastases of carcinomas of breast,
ovary, colon);
• infections (e.g. tuberculosis);
• others (e.g. pancreatic disease, ovarian disease, myxoedema)

22
Q

Benign primary liver tumours

A

haemangiomas (most common);• adenomas (C);• cysts;• focal nodular hyperplasia;• fibromas;• leiyomyomas.

23
Q

malignant primary liver tumours

A

hepatocellular carcinoma (accounts for 90 per cent of primary liver tumours);• cholangiocarcinoma;• angiosarcoma (A);• hepatoblastoma (D);• fibrosarcoma (B);• leiyomyosarcoma (E).