Practice Paper 4 Flashcards
1
Q
Whats the mx of pulmonary embolism?
A
Primary Prevention
Compression stockings
Heparin prophylaxis for those at risk
Good mobilisation and adequate hydration
If haemodynamically stable O2
Anticoagulation with heparin or LMWH *
Switch over to oral warfarin* for at least 3 months
Maintain INR 2-3 Analgesia
If haemodynamically UNSTABLE (massive PE) Resuscitate
O2
IV fluids
Thrombolysis with tPA* may be considered if cardiac arrest is imminent
Surgical or radiological
Embolectomy
2
Q
Recognise the signs of pulmonary embolism on physical examination
A
Recognise the signs of pulmonary embolism on physical examination
Severity of PE can be assessed based on associated signs:
SMALL - often no clinical signs.
There may be some tachycardia and tachypnoea
MODERATE Tachypnoea Tachycardia Pleural rub Low O2 saturation (despite O2 supplementation) **
MASSIVE PE Shock Cyanosis Signs of right heart strain ** Raised JVP ** Left parasternal heave Accentuated S2 heart sound **
MULTIPLE RECURRENT PE
Signs of pulmonary hypertension
Signs of right heart failure
3
Q
35yo woman presents with a rash under the axilla
Its dark and velvety texture
pmh of diabetes
A
Acanthosis Nigricans
(sign of severe insulin resistance) - velvety thickening and hyperpigmentation of the skin of the axillar or neck
4
Q
Which score is used to asses the risk of an adverse outcome following an upper GI bleed
A
Rockall score
o Scores the severity after a GI bleed
o Score < 3 carries good prognosis
o Score > 8 carries high risk of mortality
5
Q
64yo male presents to a&e with large rectal bleed left sided abdominal pain long history of constipation and is febrile and tachycardic
A
diverticulitis
6
Q
What’s the aetiology of diverticula?
A
There is hypertrophy of the muscles resulting in high intraluminal pressure
This leads to herniation of the mucosa at potential sited of weakness in the bowell wall ie: points of entry of blood vessels.
LAZ:
• Aetiology:
o A low-fibre diet leads to loss of stool bulk
o This leads to the generation of high colonic intraluminal pressures to propel the stool out
o This, in turn, leads to the herniation of the mucosa and submucosa through the muscularis
7
Q
What classification is used for acute diverticulitis?
A
Hinchey Classification of Acute Diverticulitis:
• Ia: phlegmon
• Ib and II: localised abscesses
• III: perforation and purulent peritonitis
• IV: faecal peritonitis
8
Q
What’s the pathogenesis of diverticulitis
A
• Pathogenesis:
o Diveticulae are most commonly found in the sigmoid and descending colon
o However, they can also be right-sided
o Diverticulae are NOT found in the rectum
o Diverticular are found particularly at sites of nutrient artery penetration
o Diverticular obstruction by thickened faeces can lead to bacterial overgrowth, toxin production and mucosal injury
o Which can then lead to diverticulitis, perforation, pericolic phlegmon, abscess, ulceration and fistulation or stricture formation
9
Q
Summarise the epidemiology of diverticular disease
A
- Diverticular disease is VERY COMMON
- 60% of people living in industrialised countries will develop colonic diverticulae
- Rare < 40 yrs
- RightMsided diverticulae are more common in Asia
10
Q
Recognise the presenting symptoms of diverticular disease
A
• Often ASYMPTOMATIC (80M90%)
• Complications can lead to symptoms such as:
o PR bleeding
o Diverticulitis (causing LIF and lower abdominal pain and fever)
o Diverticular fistulation (causing pneumaturia, faecaluria and recurrent UTI)
11
Q
Identify appropriate investigations for diverticular disease
A
Identify appropriate investigations for diverticular disease
BLOODS:
o FBC: increased WCC, increased CRP
o Check clotting and crossMmatch if bleeding
BARIUM ENEMA (with or without air contrast):
o Shows presence of diverticulae (saw-tooth appearance of lumen) **
o This reflects pseudohypertrohy of circular muscle
o IMPORTANT: barium enema should NOT be performed in the acute setting because there is a high risk of perforation
FLEX SIG AND COLONOSCOPY
o Diverticulae can be visualised and other pathology (e.g. polyps and tumours) can be excluded
ACUTE SETTING:
CT scan for evidence of diverticular disease and complications may
be performed
12
Q
How do diverticulae present on barium enema scans?
A
saw tooth apearance of lumen
13
Q
What’s the mx plan for diverticulitis?
A
• Diverticulitis: o IV antibiotics o IV fluid rehydration o Bowel rest o Abscesses ma be drained by radiologically sited drains
14
Q
Generate a management plan for asymptomatic diverticular disease
A
o Soluble high-fibre diet (20M30 g/day)
o Some drugs are under investigation for their use in preventing recurrent flares of diverticulitis (such as probiotics and anti-inflammatories)
15
Q
Identify the possible complications of diverticular disease
A
- Diverticulitis
- Pericolic abscess
- Perforation
- Faecal peritonitis
- Colonic obstruction
- Fistula formation (bladder, small intestine, vagina)
- Haemorrhage
16
Q
Define haemochromatosis
A
• An autosomal recessive disease in which increased intestinal absorption of iron causes accumulation of iron in tissues, which may lead to organ damage.
17
Q
Typical haemochromatosis presentation
A
Bronze (tan) skin pigmentation
Hepatomegaly
Diabetes mellitus background
18
Q
Explain the aetiology/risk factors of haemochromatosis
A
Explain the aetiology/risk factors of haemochromatosis
• Autosomal recessive
• Caused be a defect in the HFE gene (used to screen family members)
19
Q
What are the late symptoms of haemochromatosis?
A
o Diabetes mellitus ** o Bronzed / tan skin ****** o Hepatomegaly ** o Impotence o Amenorrhoea o Hypogonadism o Cirrhosis o Cardiac - arrhythmias* and cardiomyopathy o Neurological and psychiatric problems
20
Q
Identify appropriate investigations for haemochromatosis
A
HAEMATINICS***
serum ferritin (HIGH),
transferrin (LOW),
transferrin saturation (HIGH),
TIBC (LOW)
o NOTE: serum ferritin is NOT very specific because it is an acute phase protein
o Serum iron concentration and transferrin saturation do NOT accurately reflect total body iron stores
21
Q
Patient in post op ward presents with
vomiting, small pupils and respiratory depression
what are you thinking
A
opiate use/withdraw
Effects: euphoria nausea and vomiting constipation anorexia hypotension respiratory depression* pinpoint pupils* tremor erectile dysfunction
22
Q
What is given as an antidote for opiate withdraws?
A
Naloxone
23
Q
What are the effects of opiate WITHDRAWS?
A
dilated pupils* lacrimation sweating diarrhoea insomnia tachycardia abdominal carmp like pains* nausa and vomiting
24
Q
How is opiate dependance managed
A
methadone
buprenorphine
25
Whats the difference regarding pupil presentation in opiate USE and opiate WITHDRAW?
opiate use = pinpoint
| opiate withdraws = dilated
26
What does GTN spray do ?
It causes peripheral vasodilatation reducing afterload and resting her myocardium
27
What are you thinking for a pt with "sob on exertion" with normal ecg normal bloods normal xray.
stable angina
28
Which AB are contraindicated for pregnancy?
Ciprofloxacin - quinolone - development of arhtropathy in a child
Trimethoprim - folate antagonist - risk of teratogenicity
29
Which AB can be used in pregnancy?
Co-amoxiclav
| Penicillins
30
What does a pansystolic murmur indicate?
Mitral regurgiation - left ventricular dilatation
31
What do you expect to find on an ECG for left ventricular hypertrophy?
o Hypertrophic
• LeftMaxis deviation
• Signs of left ventricular hypertrophy
• Q waves in inferior and lateral leads
32
What is polycystic kidney disease
Autosomal dominant inherited disorder characterised by the development of multiple renal cysts that gradually expand and replace normal kidney substance, variablyas
33
What are the genetics of PKD?
85% caused by mutations in PKD1 on chromosome 16
This is a membrane-bound multidomain protein involved in cell-cell and cell-matrix interactions
15% caused by mutations of PKD2 on chromosome 4
34
Whats the pathophysiology of PKD?
Pathophysiology
Proliferative/hyperplastic abnormality of the tubular epithelium
Early on, the cysts are connected to the tubules from which they arise and thefluid content is glomerular filtrate
When cyst diameter >2 mm, they detach from the tubule and the fluid content isderived from secretion of the lining epithelium
With time, the cysts enlarge and cause progressive damage to adjacent functioning nephrons
35
Summarise the epidemiology of polycystic kidney disease
MOST COMMON inherited kidney disorder
| Responsible for 10% of end-stage renal failure
36
Recognise the presenting symptoms of polycystic kidney disease
Present at 30-40 yrs*
20% have no family history
May be asymptomatic
Flank Pain - may result from cyst enlargement/bleeding, stone, blood clot migration,infection
Haematuria*
Hypertension
Associated with berry aneurysms and may present with subarachnoid haemorrhage
37
Recognise the findings OE for PKD
Abdominal distension
Enlarged cystic kidneys - palbable masses in flanks
Palpable liver Hypertension
Signs of chronic renal failure (at late stage)
AAA signs
38
Identify appropriate IX for PKD
US or CT
Multiple cysts bilaterally
Liver cysts
39
What's the treatment of status epilepticus?
IV lorazepam (or PR) and repeat every 10
then
IV phenytoin
then consider GA
40
What is a classic status epilepticus presentation?
Homeless alcoholic found seizing for more than 30 mins
41
What's the antidote for paracetamol?
N-acetylcysteine
42
Recognise the signs of paracetamol overdose on physical examination
* 0-24 hrs - no signs
* 24-72 hrs - liver enlargement and tenderness
* 72+ hrs - jaundice, coagulopathy, hypoglycaemia, renal angle tenderness
43
What's the first line treatment of massive PE?
dose of LMWH then warfarin
| then consider thrombolysis (if the pt has no haemorrhagiv risk
44
Whats the treatment for H Pylori? And for how long
TRIPLE THERAPY:
PPI
Metronidazole
Clarithromycin
for 1-2 weeka
45
What is Zollinger-Ellison syndrome?
RARE cause of ulcer disease
A condition in which a gastrin-secreting tumour or hyperplasia of the islet cells in the pancreas cause overproduction of gastric acid, resulting in recurrent peptic ulcers
46
What differs between pc of duodenal and gastric ulcer?S
Symptoms have a variable relationship to food intake:
o Gastric - pain is worse SOON after eating
o Duodenal - pain is worse SEVERAL AFTERS HOURS eating
47
What ix do you do for H pylori
• Testing for H. pylori:
o C13-urea breath test :
• RadioMlabelled urea is given by mouth
• C13 is detected in the expelled air
o Serology:
• IgG antibody against H. pylori confirms exposure to H. pylori but NOT eradication
o Campylobacter-like organism (CLO) test:
• Gastric biopsy is placed with a substrate of urea and a pH indicator
• If H. pylori is present, ammonia is produced from the urea and there is a colour change from yellow to red
48
```
Pt comes in following a fall
He is a smoker
o2 sats 76%
ABG: ph normal, po2 low, pco2 high, hco3 high.
What are you thinking?
```
Smoker = suggests COPD
high paco2 and low po2 = type 2 resp failure
which can lead to respiratory acidosis
which is then compensates by hco3 (thats why ph is normal)
49
What does a raised unconjugated bil indicate?
Either increase rate of Hb breakdown to unc bil
OR
Innability of liver to conjugate bil fast enough
(gilberts syndrome = hereditary deficiency of enzymes which conjugate bilirubing)
50
What does a raised conjugated bil indicate?
It indicates that the liver is working fine - conjugating bil as it should and that there is an obstruction further down
In liver and bile ducts.
51
What's haemolytic anemia?
• Premature erythrocyte breakdown causing shortened erythrocyte life span (< 120 days) with anaemia
A pre hepatic cause of jaundice
A shortened erythrocyte life span means more breakdown products are presents such as unconjugated bilirubin.
52
What causes haemolytic anemia?
HEREDITARY
o Membrane Defects
• Hereditary spherocytosis
• Elliptocytosis
o Metabolic Defects
• G6PD deficiency
• Pyruvate kinase deficiency
o Haemoglobinopathies
• Sickle cell disease
• Thalassemia
ACQUIRED
o Autoimmune
• Antibodies attach to erythrocytes causing intravascular and extravascular haemolysis
o Isoimmune
• Transfusion reaction
• Haemolytic disease of the newborn
```
o Drugs
• Penicillin
• Quinine
• NOTE: this is caused by the formation of a drug-antibody-erythrocyte
complex
```
o Trauma
• Microangiopathic haemolytic anaemia (caused by RBC fragmentation in abnormal microcirculation)
! E.g. haemolytic uraemic syndrome, DIC, malignant hypertension
o Infection
• Malaria
• Sepsis
o Paroxysmal nocturnal haemoglobinuria
53
Summarise the epidemiology of haemolytic anaemia
* COMMON
* Genetic causes are prevalent if African, Mediterranean and Middle Eastern populations
* Hereditary spherocytosis is the most common inherited haemolytic anaemia in northern Europe
54
Recognise the presenting symptoms of haemolytic anaemia
* Jaundice
* Haematuria
* Anaemia
55
Recognise the signs of haemolytic anaemia on physical examination
* Pallor
* Jaundice
* Hepatosplenomegaly
56
Identify appropriate investigations for haemolytic anaemia
• Bloods
o FBC:
• Low Hb
```
BLOODS
o FBC:
• Low Hb *
• High reticulocytes *
• High MCV *
• High unconjugated bilirubin *
• Low haptoglobin (a protein that binds to free Hb released by red blood cells)
```
o U&Es
o Folate
```
BLOOD FILM
o Leucoerythroblastic picture
o Macrocytosis
o Nucleated erythrocytes or reticulocytes
o Polychromasia
o May identify specific abnormal cells such as:
• Spherocytes
• Elliptocytes
• Sickle cells
• Schistocytes
• Malarial parasites
```
URINE
o High urobilinogen
o Haemoglobinuria
o Haemosiderinuria
• Direct Coombs' Test
o Tests for autoimmune haemolytic anaemia
o Identifies erythrocytes coated with antibodies
• Osmotic fragility test or Spectrin mutation analysis
o Identifies membrane a§bnormalities
• Ham's Test
o Lysis of erythrocytes in acidified serum in paroxysmal nocturnal haemoglobinuria
• Hb Electrophoresis or Enzyme Assays
o To exclude other causes
• Bone Marrow Biopsy (rarely performed)
57
What's the signifigance of haptoglobin in haemolytic anaemia?
It normally binds free hb therefore levels decrease where there is increased red cell breakdown.
58
Which disease is often misdiagnosed for parkinsons?
Essential tremor/familial tremor
59
What is normal pressure hydrocephalus?
• Normal Pressure Hydrocephalus -idiopathic chronic ventricular enlargement. The long white matter tracts are damaged leading to gait and cognitive decline
consider it when someone is presenting with alzheimers and neurological symptoms and they are middle aged.
60
What is the triad of symptoms for normal pressure hydrocephalus?
* Dementia
* Gait disturbance
* Urinary incontinence
61
Recognise the signs on examination for normal pressure hydrocephalus
o Cognitive impairment
o Gait apraxia (shuffling)
o Hyperreflexia
62
32yo female presents with tingling and numbness around her mouth and painful carpal spasm.
She has recently had a subtotal thyroidectomy for graves
What are you thinking and why?
Hypocalcemia
Is common in subtotal thyroidectomies
Reduced PTH = low ca & high phosphate
63
What are the pc of hypocalcemia?
Perioral parashesia
Muscular cramping
Depression
64
What are the signs OE of hypocalcaemia?
Trousseaus sign = inflate bp cuff and carpopedal spasm is induced
Chvostek's sign = facial twitching when the facial nerve is excited by tapping above the parotid gland.
65
What is the mx for mild hypocalcemia?
oral calcium supplements
66
Whats the mx for acute hypocalcemia?
10ml intravenous dose of 10% calcium gluconate
67
State some causes of hypocalcemia
```
Alkalosis
vit d deficiency
chronic renal failure
pseudohypoparathyroidism
acute pancreatitis
hypomagnesaemia
```
68
62yo female presents with a collapse in a&e
She felt dizzy on standing up from a sitting position
She complains of fatigue the past month
She has a high sodium and low K level
What are you suspecting
Adrenocortical insufficiency
Do synACTHten test
69
What is delirium tremens
Acute alcohol withdrawal
Includes severe delirium
Has high mortality
70
What is the result you expect in poor liver function?
Prolonged prothrombin time
A raised albumin indicates an acute phase protein
71
What does a raised ALP and ALT indicate?
Markers of hepatocellular damage
| mechanical damage to the liver
72
What is bronchiecstasis?
An abnormal permanent dilatation of bronchi secondary to destruction of the bronchial wall
It is usually acquired as a consequence of recurrent infections or severe ones.
73
How do pts typically present with bronchiectasis?
Chronic cough
Large amounts of sputum
Sometimes haemoptysis
74
What are the classic sings of bronchiectasis OE?
Inspiratory squeaks an crackles over the hila
75
What do you expect to find on an CXR of a bronchiectasis pt
Dilated bronchi (may be seen as parallel lines going
from the hilum to the diaphragm (tramline shadows))
Fibrosis
Atelectasis
Pneumonic consolidations
May be NORMAL
Hyperinflated chest
76
Define stroke
Rapid permanent neurological deficit from cerebrovascular insult. Also defined clinically, as focal or global impairment of CNS function developing rapidly and lasting > 24 hrs
• Can be subdivided based on:
o Location - anterior circulation vs posterior circulation
o Pathological Process - infarction vs haemorrhage
77
What causes an infarction stroke?
• INFARCTION (80%)
o Thrombosis
• Can occur in small vessels (lacunar infarcts)
• Can occur in larger vessels (e.g. middle cerebral artery)
• Can arise in prothrombotic states (e.g. dehydration, thrombophilia)
o Emboli
• From carotid dissection, carotid atherosclerosis, atrial fibrillation
• NOTE: they can arise from venous blood clots that pass through a septal
defect (e.g. VSD) and get lodged in the cerebral circulation
o Hypotension
• If the blood pressure is below the autoregulatory range required to maintain cerebral blood flow, you can get infarction in the watershed zones between different cerebral artery territories
o Others
• Vasculitis
• Cocaine (arterial spasm)
78
What causes a haemorrhagic stroke?
o Hypertension
o CharcotMBouchard microaneurysm rupture (DEFINITION: aneurysms within the brain vasculature that occur in small blood vessels)
o Amyloid angiopathy
o Arteriovenous malformations
o Less common: trauma, tumours, vasculitis
79
PC of stroke
SUDDEN ONSET
• Weakness
• Sensory, visual or cognitive impairment
• Impaired coordination
• Impaired consciousness
• Head or neck pain (if carotid or vertebral artery dissection)
• Enquire about time of onset (critical for emergency management if < 4.5 hrs)
• Enquire about history of AF, MI, valvular heart disease, carotid artery stenosis, recent neck trauma or pain
80
Generate a management plan for HYPERACUTE STROKE
o If < 4.5 hrs from onset
o Exclude haemorrhage using CT-head
o If haemorrhage excluded, thrombolysis may be considered
81
What ix will you do for a stroke?
```
Bloods
CT/MRI
ECG
Echo
Carotid doppler US
```
82
What is the mx for ACUTE ISCHAEMIC STROKE
o Aspirin + Clopidogrel to prevent further thrombosis (once haemorrhage excluded on CT head)
o Heparin anticoagulation considered if there is a high risk of emboli recurrence or stroke progression
o Formal swallow assessment (NG tube may be needed) o GCS monitoring
o Thromboprophylaxis
83
Identify the possible complications of stroke
* Cerebral oedema (increased ICP)
* Immobility
* Infections
* DVT
* Cardiovascular events
* Death
84
Whats the ABCDE rule for malignant melanoma
```
Asymmetry
Border irregularity
Colour irregularity (within the mole)
Diameter >7mm
Evolution of lesion (size, shape, colour)
```
If the mole in question is simply a different shade than other moles - is not a concering feature. This is normal, all moles we have are a slightly different shade.
85
Which concerning features of a mole will point towards malignant melanoma?
```
Itchy
Bleeding
Oozing
Elevation
Altered sensation
```
86
What are the RF for malignant melanoma?
SUN EXPOSURE** as a child "from australia"
Type 1 skin
FH
87
Whats the most common type of breast cancer
Invasive ductal carcinoma
88
Explain the aetiology/risk factors of breast cancer
```
• Genetics (e.g. BRCAM1 and BRCAM2 genes)
• Environmental factors
• Risk Factors
o Age
o Prolonged exposure to oestrogen
• Nulliparity (not having kids)
• Early menarche
• Late menopause
• Obesity
• COCP
• HRT
o Family history of breast cancer
```
89
What age group has the peak incidence of brc?
40-70yo
90
Recognise the presenting symptoms of breast cancer
* Breast lump (usually painless)
* Changes in breast shape
* Nipple discharge (may be bloody)
* Axillary lump
```
+FLAWS
• Symptoms of malignancy:
o Weight loss
o Bone pain
o Paraneoplastic syndrom
```
91
What are the cardinal features of hyperprolactinaemia?
```
Galactorrhea
Hypogonadism=
2' amenorrhoea
anovulation
infertility
(decreased libido and lethargy in men)
```
92
Which drug is known to cause hyperprolactinaemia?
Dopamine antagonists
ie: antipsychotics, antidepressants, antiemetics
are known to increase prolactin concentration
93
Hyperthyroidism pc
* Weight loss despite increased appetite
* Irritability
* Weakness
* Diarrhoea
* Sweating
* Intermittent Palpitations
* Tremor
* Anxiety
* Heat intolerance
* Loss of libido
* Oligomenorrhoea/amenorrhoea
94
Whats the most common cause of hyperthyroidism?
GRAVES
| tsh receptor antibodies.
95
Recognise the signs of Graves disease on physical examination
* Palmar erythema
* Sweaty and warm palms
* Fine tremor
* Tachycardia (may be AF)
* Hair thinning
* Urticaria/pruritus
* Brisk reflexes
* Goitre
* Proximal myopathy
* Lid lag
* Gynaecomastia
96
Identify appropriate investigations for Graves disease
• TFTs - low TSH + high T3/T4
• Autoantibodies
o Anti-TPO antibodies ** (thyroid peroxidase) - found in 75% of Graves
o Anti-thyroglobulin antibodies
o TSH-receptor antibodies M very sensitive and specific for Graves
• Imaging
o Thyroid ultrasound
o Thyroid uptake scan
• Inflammatory Markers - CRP/ESR will be raised in subacute thyroiditis
97
```
33yo male presents with
worstening headaches and tiredness
good apettite & weight gain
Difficulty biting his food
OE: tall, oval shaped face, large hands, prominent jaw
What are you thinking
```
Acromegaly
98
What is acromegaly?
• Constellation of signs and symptoms caused by hypersecretion of GH in adults
o Excess GH before puberty results in GIGANTISM
99
What are the most common causes of acromegaly
* Most cases are caused by a GH-secreting pituitary adenoma
* RARELY caused by excess GHRH causing somatotroph hyperplasia from hypothalamic ganglioneuroma, bronchial carcinoid or pancreatic tumours
100
Recognise the presenting symptoms of acromegaly
```
• Very gradual progression of symptoms over many years • Rings and shoes becoming tight
• Increased sweating
• Headaches *
• Carpal tunnel syndrome
• Hypopituitary symptoms:
o Hypogonadism
o Hypothyroidism
o Hypoadrenalism
• Visual disturbances (due to compression of optic chiasm by tumour)
• Hyperprolactinaemia leading to:
o Irregular periods
o Decreased libido
o Impotence
```
101
Recognise the signs of acromegaly on physical examination
```
• Hands
o Large spade-like hands
o Thick greasy skin
o Carpel tunnel syndrome signs
o Premature osteoarthritis
```
```
• Face
o Prominent eyebrow ridge
o Prominent cheeks
o Broad nose bridge
o Prominent nasolabial folds
o Thick lips
o Increased gap between teeth
o Large tongue
o Prognathism
o Husky resonant voice (due to thickening of vocal cords)
```
• Visual Field Loss
o Bitemporal superior quadrantopia progressing to bitemporal hemianopia
• Neck
o Multinodular goitre
• Feet
o Enlarged
102
Identify appropriate investigations for acromegaly
• Serum IGFJ1 M useful screening test
o GH stimulates IGFM1 secretion
• Oral Glucose Tolerance Test (OGTT) **
o Positive result: failure of suppression of GH after 75 g oral glucose load
```
• Pituitary Function Tests
o 9am cortisol
o Free T4 and TSH
o LH and FSH
o Testosterone
o Prolactin
```
• MRI of Brain M visualise the pituitary adenoma
103
Mx of acromegaly
* Surgical - trans-sphenoidal hypophysectomy
* Radiotherapy - adjunctive to surgery
• Medical - if surgery is contraindicated or refused
o Subcutaneous Somatostatin Analogues
• Examples: octreotide, lanreotide **
• Side-effects: abdominal pain, steatorrhoea, glucose intolerance, gallstones
o Oral Dopamine Agonists
• Examples: bromocriptine, cabergoline **
• Side-effects: nausea, vomiting, constipation, postural hypotension, psychosis (RARE)
o GH Antagonist (pegvisomant)
o Monitor
• GH and IGF1 levels can be used to monitor disease control
104
Complications of acromegaly
• CVS
o Cardiomegaly
o Hypertension
• Respiratory
o Obstructive sleep apnoea
• GI
o Colonic polyps
```
• Reproductive
o Hyperprolactinaemia (in 30% of cases)
```
```
• Metabolic
o Hypercalcaemia
o Hyperphosphataemia
o Renal stones
o Diabetes mellitus
o Hypertriglyceridaemia
```
• Psychological
o Depression
o Psychosis (from dopamine agonists)
```
• Complications of Surgery
o Nasoseptal perforation
o Hypopituitarism
o Adenoma recurrence
o CSF leak
o Infection
```
105
Prognosis of acromegaly
Summarise the prognosis for patients with acromegaly
• GOOD with early diagnosis and treatment
• Physical changes are irreversible
106
Which drugs need to be lowered in renal failure?
NSAIDS = nephrotoxic (diclofenac)
Digoxin = toxicity and impairment
Furosemide = potent diuretic
Metformin = metabolic acidosis (when u have increasd creatinine)
ACEi - we dont want to further renal function
b-blockers
107
What should you immediately think with rectal bleeding of fresh blood associated with sharp pain and use of strong anelgesia for an unrelated injury?
ANAL FISSURES
Fresh blood through anus = fissures, burst haemorrhoids (crohn's)
Unbearable sharp pain on defacation = fissure
Recent opiate use = constipation
EXPLANATION: opiates cause constipation which requires straining to defacate. Straining makes you prone to fissures.
108
What does Kayser Fleischer rings look like
| What does it indicate
green yellow discolouration around the iris
- seen during slit lamp examination.
wilson's disease
109
What is wilsons disease
COPPER deposition in vital organs due to error in metabolism
LAZ:
An autosomal recessive disorder characterised by reduced biliary excretion of copper
and accumulation of copper in the liver and brain, especially in the basal ganglia. Also
known as hepatolenticular degeneration.
110
How would a child/young adult present with Wilson's?
Neurological changes = "not herself lately" "behavioural changes
+ kaiser fleischer rings
111
Identify appropriate investigations for Wilson's disease
• Bloods
o LFTs: high AST, ALT, ALP
o Low serum caeruloplasmin
• NOTE: caeruloplasmin is an acute phase protein so may give false-negatives if there is an underlying infectious/inflammatory process
o Serum copper **
• 24 hour urinary copper levels M increased in Wilson's disease
• Liver biopsy - increased copper content
• Genetic analysis - Wilson's is caused by a wide variety of gene mutations so there isn't a simple genetic test that can be done
112
What is a classic dermatological sign of SLE?
Malar rsh - red rash across the cheeks
| important for making a diagnosis
113
How does a patient present with SLE?
Very vague symptoms like malaise, weight loss etc
| MALAR RASH IS KEY
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What are the CRP levels in SLE?
normal !
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Which auto antibodies do you expect to find for SLE?
o Anti-dsDNA (60%)
o Rheumatoid factor (30-50%)
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o Anti-ENA
o Anti-RNP
o Anti-SM
o Anti-Ro
o Anti-La
o Anti-histone
o Anti-cardiolipin
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What are the symptoms of uraemia?
subtle pale yellow shade of skin "lemon yellow"
Uraemic encephalopathy = cloudy consciousness
Acute confusional state
Myoclonic jerks which can progress to seizures
Hiccoughing is also seen
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When do you expect to see spider naevi?
in chronic liver disease
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Where is ADH secreted from?
| When is ADH secreted?
From the posterior pituitary fland
| In response to high plasma osmolality, hypovolaemia or stress.
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What does ADH do in the body.
It stimulates the reabsorbtion of water from the collecting ducts of the nephron back into the circulation (to reverse high plasma osmolality and hypovolaemia)
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What is diabetes insipidus?
Decrease or lack of ADH secretion
| Nephrogenic or Cranial
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How does diabetes insipidus present?
massive polyuria and polydipsia
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How is diabetes insipidus usually diagnosed?
By the water deprivation test
This involves measuring the patients urine volume, concentration and plasma osmolality whilst depriving them of water.
POSITIVE RESULT = when the water deprivation test fails to INCREASE the concentration of urine - due to a lack of ADH or insensititivy to its actions.
Then to differentiate between nephrogenic and cranial:
You give them desmopressin and if they concentrate their urine in response its cranial if not it's nephrogenic.
