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A. REVISION FROM QBANKS > 17/10/2024 > Flashcards

17/10/2024 Flashcards

1
Q

Which cancer is Hashimoto’s thyroiditis associated with?

A

MALT lymphoma

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2
Q

What biologic therapies are indicated for crohns and rheumatoid diseases?

A

TNF alpha inhibitors

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3
Q

Examples of TNF alpha inhibitors?

A

Adalimumab
Infliximab
Etanercept

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4
Q

What biologic therapies are indicated for CMl and GI stromal tumours?

A

Tyrosine kinase inhibitors

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5
Q

Example of tyrosine kinase inhibitor?

A

Imatinib

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6
Q

Management of uterine fibroids?

A

Medical with GnRH agonists in the short term to shrink the fibroids
Surgical is long term e.g. myomectomy, hysterectomy, hysteroscopic endometrial ablation or uterine artery embolisation

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7
Q

Is TLCO up or down in emphysema?

A

Down as the damage to the alveoli means reduced area for gas exchange to occur

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8
Q

What are 95% of gastric MALT lymphomas associated with?

A

H.pylori

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9
Q

Tx of gastric MALT lymphoma?

A

H.pylori eradication e.g. PPI & amoxillin & clarithromycin

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10
Q

In what circumstance can testicular torsion have a persevered cremasteric reflex?

A

When there is torsion of the testicular appendage

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11
Q

Whats the most common cancer in men aged 20-30?

A

Testicular cancer

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12
Q

Most common type of testicular cancer?

A

Seminomas

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13
Q

Which markers are raised in Seminomas in testicular cancer?

A

HCG and LDH

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14
Q

How do you carry out the cremasteric reflex?

A

stroking the inner aspect of the thigh towards the groin, which causes the cremasteric muscle within the scrotum to contract and thereby elevate the ipsilateral testis and scrotum.

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15
Q

In the management of DKA, at what point would you add 10% dextrose?

A

When blood glucose is <14mmol/L

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16
Q

What is the definition of resolution of DKA?

A

PH >7.3
Ketones <0.6
Bicarbonate >15

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17
Q

By how much does Barrett’s oesophagus increase the risk of oesophageal adenocarcinoma?

A

50-100 fold increased risk

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18
Q

Is Barrett’s symptomatic?

A

No but most pts have concurrent GORD

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19
Q

Outline management of Barrett’s oesophagus?

A

Lifestyle: weight loss, stop smoking, small regular meals etc
High dose PPI e.g. 40mg BD esomeprazole
Endoscopic surveillance every 2-3 years if long-segment or 3-5 years if short segment (i.e. <3cm)

If dysplasia is ever found then endoscopic Tx with ablation or mucosal resection is done

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20
Q

What is the HbA1c of pre-diabetes>?

A

42-47mmol/mol

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21
Q

What is impaired fasting glucose?

A

Fasting glucose level of 6.1-6.9 - a form of pre-diabetes
Due to hepatic insulin resistance

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22
Q

What is impaired glucose tolerance?

A

An OGTT test result of 2 hour blood glucose of 7.9-11.0 or a fasdting glucose of <7.0
A form of pre-diabetes
Due to muscle insulin resistance

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23
Q

Tx of first degree heart block?

A

asymptomatic first-degree heart block is relatively common and does not need treatment

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24
Q

Outline the 2 types of second-degree heart block?

A

type 1 (Mobitz I, Wenckebach): progressive prolongation of the PR interval until a dropped beat occurs
type 2 (Mobitz II): PR interval is constant but the P wave is often not followed by a QRS complex

25
Q

What is the characteristic ecg finding in first-degree heart block?

A

PR interval >200ms (<5 small squares)

26
Q

Management of status epilepticus in hospital ?

A

IV lorazepam is usually used. Can be repeated once after 5-10 minutes
If ongoing then consider second line - levetiracetam (or..phenytoin or sodium valproate)
If refractory status (no response within 45 minutes from onset) - induction of GA or phenobarbital

27
Q

Amnagement of autoimmune encephalitis?

A

IV aciclovir is usually started in all cases of suspect encephalitis

If autoimmune is suspected them steroids and IV immunoglobulins

28
Q

Which subtype of breast cancer usually causes an abnormal proliferation of small, round cells arranged in a uniform pattern?

A

Lobular carcinoma

29
Q

Which subtype of breast cancer usually causes irregularly distributed cells with atypically large nuclei?

A

Ductal carcinoma

30
Q

Investigations for endometriosis?

A

Urine pregnancy test
TVUS is unlikely to show anything but is important to screen for other pathology so if Sx are significant pt should be referred for a laparoscopy as the gold-standard investigation

31
Q

Management of endometriosis-related pain?

A

Consider short trial of paracetamol and/or NSAID
If this doesnt help then -> hormonal treatment e.g. COCP or progestogen

If this doesnt work then refer to secondary care

32
Q

Secondary care management options for endometriosis?

A

Medical:
GnRH analogues can be used to induce a pseudo menopause - note this doesnt have a significant impact on fertility rates

Surgical:
Laparoscopic excision or ablation of endometriosis + adhesiolysis - has shown to improve chances of conception
Ovarian cystectomy for endometriomas is recommended
Hysterectomy performed laparoscopically may be done

33
Q

What is surgical menopause?

A

If your ovaries are removed during a hysterectomy, you’ll go through the menopause immediately after the operation, regardless of your age. This is known as a surgical menopause.

Hysterectomy with oophorectomy: Immediate surgical menopause because no ovaries = no hormones.
Hysterectomy without oophorectomy: No periods, but not necessarily in menopause until the ovaries stop producing hormones, which may happen earlier due to the surgery.

34
Q

Serum osmolality in HHS?

A

> 320

35
Q

Management of secretions in palliative care?

A

Avoid fluid overload and educate family that pt is not likely troubled by secretions

hyoscine hydrobromide or hyoscine butylbromide is generally used first-line (these are Anticholinergics)

36
Q

What % of IgA nephropathy pts will progress to end stage renal disease in 10-25 years?

A

30%

37
Q

What are the types of polycthemia?

A

Relative e.g. dehydration or stress in gaisbock syndrome
Primary i.e. polycythemia rubra vera
Secondary e.g. COPD, high altitude, OSA, excessive EPO in renal cancer, hepatoma etc

38
Q

How can you differentiate between true polycythemia and relative polycythemia?

A

Red cell mass studies can be used
In true polycythaemia the total red cell mass in males > 35 ml/kg and in women > 32 ml/kg whereas in relative there isnt actually any increase in RBCs so red cell mass would be normal

39
Q

What is polycythemia vera?

A

A myeloproliferative disorder caused by clonal proliferation of a marrow stem cell leading to an increase in red cell volume.
Most cases have a mutation in JAK2
Rare and tends to present in adults 60-70

40
Q

Sx of polycthemia vera?

A

pruritus, typically after a hot bath
Headaches, dizziness and sweating
Fatigue
Tinnitus
Erythromelalgia: burning pain, warmth and redness in hands and feet
Ruddy complexion
Blurred vision temporarily due to hyper-viscosity
Gout
splenomegaly
hypertension
hyperviscosity: some pts present with arterial and venous thrombosis]

If secondary…
Loom for Sx of COPD, OSA, renal artery stenosis or renal tumours and hepatomas.

41
Q

What is secondary polycythemia?

A

When a high number of erythrocytes are produced in a physiological response to chronic hypoxia (COPD etc), local renal hypoxia or excess EPO production i.e. secondary to EPO-secreting tumours

42
Q

What investigations should be performed for suspected polycythemia vera?

A

Urinalysis for secondary renal causes
FBC - Hb and haematocrit raised. Also likely to see a rise in neutrophils and thrombocytes
Blood film - assess for features of leukaemia
JAk2 mutation
Serum ferritin - should be normal or low due to increased demand for iron
U&Es
LFTs
Serum EPO

43
Q

How is polycthemia vera treated in secondary care?

A

Venesection to maintain haematocrit <0.45
Aspirin 75mg daily and if considered high risk of thrombosis pharmacological cytoreductive therapy is recommended e.g. hydroxycarbamide

44
Q

Prognosis of polycthemia vera?

A

thrombotic events are a significant cause of morbidity and mortality
5-15% of patients progress to myelofibrosis
5-15% of patients progress to acute leukaemia (risk increased with chemotherapy treatment)

45
Q

How can doxazosin cause postural hypotension?

A

It’s an alpha blocker so it inhibits postsynaptic alpha 1 receptors on vascular smooth muscles = decreases systemic peripheral vascular resistance = reducing blood pressure

46
Q

Most common precipitating factor for digoxin toxicity?

A

Hypokalaemia - digoxin normally binds to the ATPase pump on the same site as potassium. Hypokalaemia → digoxin more easily bind to the ATPase pump → increased inhibitory effects
This is why drugs like thiazide & loop diuretics can precipitate it

47
Q

Tx of digoxin toxicity?

A

Stop digoxin
Digibind
correct arrhythmias
monitor potassium

48
Q

Causes of hyposplenism?

A

splenectomy
sickle-cell
coeliac disease & dermatitis herpetiformis
Graves’ disease
systemic lupus erythematosus
amyloid

49
Q

Blood film findings in hyposplenism?

A

Howell-jolly bodies - nuclear remnants which are usually removed by the spleen
Siderocytes and spiculated spherocytes

50
Q

What ABx can be used to treat campylobacter jejuni gastroenteritis if it’s severe?

A

Clarithromycin

51
Q

What is ovarian hyperstimulation syndrome?

A

an iatrogenic and potentially life-threatening complication of superovulation caused by vasoactive products released by hyperstimulated ovaries. This results in increased membrane permeability and loss of fluid from the intravascular compartment
It’s seen following gonadotropin or hCG treatment. Up to 1/3rd of women who are having IVF may experience a mild form of OHSS

52
Q

Risk factors for ovarian hyperstimulation syndrome?

A

Young age
Previous history of OHSS
Lean physique
PCOS
Multiple pregnancies

53
Q

Symptoms of ovarian hyperstimulation syndrome?

A

Abdominal swelling, abdominal pain, nausea and vomiting
Severe - thrombosis, renal and liver dysfunction, acute RDS

54
Q

Causes of serotonin syndrome?

A

SSRI
MAOIs
Ecstacy
Amphetamines

55
Q

Features of serotonin syndrome?

A

Within hours of taking a new drug or increasing the dose

neuromuscular excitation - hyperreflexia, myoclonus, rigidity, tremor

autonomic nervous system excitation - hyperthermia, sweating, dilated pupil

altered mental state - confusion

56
Q

Management of an acute anal fissure (<1 week Hx)?

A

Soften stool with fibre in diet, increase fluid intake and use bulk forming laxatives such as isphagula husk
Lubricants before defecation e.g. Vaseline
Topical anaesthetics can be used
Analgesia

57
Q

Management of a chronic anal fissure?

A

In addition to lifestyle…
Rectal GTN ointment to aid healing for 6-8 weeks BD
If no improvement after 8 weeks then consider secondary care referral to consider surgery (sphincterotomy) or botulinum toxin

58
Q

What is a sphincterotomy?

A

Tx of anal fissures
Makes a small cut to reach anal sphincter. Small cut in sphincter to relax it and stop it going into spasm which will allow the fissure to heal

A. REVISION FROM QBANKS (11 decks)

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