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GEM > FFP Medicine > Flashcards

FFP Medicine Flashcards

1
Q

Left vs right bundle branch block

A

Left block. WiLLiaM : W in V1 M in V6 (with inverted t wave

Right block. MaRRoW : M in V1 W in V6

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2
Q

If giving 30% oxygen, what should PaO2 be ?

A

20

Should be 10 less than that given

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3
Q

Anion Gap

A

Metabolic acidosis
Gap between positive and negative ions

11-18: Loss of HCO3
Renal tubular acidosis, diarrhoea, drugs, pamcreatic intestinal fissure

18<: Production of organic acids
lactic acidosis, ketosis, urate, drugs e.g. NSAIDs

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4
Q

Common Symptoms of GORD

A

heartburn (an uncomfortable burning sensation in the chest that often occurs after eating)
acid reflux (where stomach acid comes back up into your mouth and causes an unpleasant, sour taste)
oesophagitis (a sore, inflamed oesophagus)
Halitosis (bad breath)
Bloating and belching
Nausea and/or vomiting
Pain when swallowing (odynophagia) and/or difficulty swallowing (dysphagia)

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5
Q

Two types of hiatus hernia

A

Sliding - abdo oesophagus and cadia displaced
Rolling/Para-oesophageal - phrenico-oesophageal lig. in place, proximal stomach displaced; more likely to strangulate

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6
Q

Complications of GORD

A

Oesophageal Ulcers (bleeding, pain, odynophagia
Oesophageal stricture (dysphagia, odynophagia)
Barrett’s Oesophagus (around 1 in 10 patients)
Metaplasia in the mucosal cells lining the lower portion of the oesophagus, from normal stratified squamous epithelium to simple columnar epithelium
Oesophageal Cancer (around 5-10% of patients with Barrett’s in 10-20 years)

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7
Q

Investigations to confirm GORD in primary care

A

Refer if:
Unsure of GORD diagnosis
Symptoms are persistent, severe or unusual
Not controlled by prescribed medication
May benefit from surgery
Signs of a potentially more severe condition, such as difficulty swallowing or unexplained weight loss
Referral guidance for endoscopy

For people presenting with dyspepsia together with significant acute gastrointestinal bleeding, refer them immediately (on the same day) to a specialist.

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8
Q

Specialist investigations for GORD

A

Oesophageal manometry and ambulatory 24-hour oesophageal pH monitoring (to quantify reflux and assess the relationship between reflux episodes and the person’s symptoms).
Barium swallow or meal (to help exclude structural disorders such as hiatus hernia or motility disorders such as achalasia).

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9
Q

Interventions for GORD

A

Offer people a full-dose PPI

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10
Q

Two types of peptic ulcer

A

Gastric Ulcer
May be more painful immediately after food
May present with small bleed (iron deficiency anaemia) or major haemorrhage (haematemesis)

Duodenal Ulcer
May improve with food (delay gastric emptying)
May present with bleeding (posterior ulcer) or perforation (anterior)

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11
Q

Causes of PUD

A

Helicobacter pylori (H. pylori) - most common
Long-term use of aspirin and nonsteroidal anti-inflammatory drugs (NSAIDs)
Long term or high dose corticosteroids
BONUS: Increase acid production (Zollinger-Ellison syndrome, gastrin producing tumour)
BONUS: Increased intracranial pressure (cushing ulcers)
BONUS: Post severe burns (Curling ulcer)

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12
Q

testing for H. pylori

A

Test for H. pylori using a carbon-13 urea breath test or a stool antigen test, or laboratory-based serology

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13
Q

What is absorbed where in small intestine

A

Duodenum – predominantly further digestion of chyme but does absorb iron, selenium, po4
Jejunum – sugars, amino acids, lipids, ca zinc folate po4
Ileum – b12 and bile acids (TI), ca, sugars, amino acids, lipids, magnesium (distal)

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14
Q

How may a patient with malabsorption present?

A

Weight loss – net loss of calories
Energy sources include fats, proteins and carbohydrates
Diarrhoea
Clinical syndrome associated with an underlying disease (e.g. features typical for Crohn’s)
Clinical syndrome caused by the loss of an essential nutrient (e.g. vitamin and mineral deficiency)

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15
Q

Investigating suspected malabsorption

A

Bloods: FBC, UE, LFT, CRP, albumin, ferritin, b12, folate, vitamin D, clotting, bone profile, selenium zinc and copper.
In addition TTG and TSH will check for causes of malabsorption
Stool: calprotectin, stool culture, faecal elastase, FIT
Imaging: imaging of pancreas or biliary tree (MRCP), MR enterography,
Endoscopy: UGI endoscopy (with d2 biopsy), capsule, colonoscopy (TI assessment)

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16
Q

Causes of malabsorption (Many)

A

Structural change to the gut (surgery or congenital)
Bariatric and UGI, whipple’s procedure (pancreas), cholecystectomy, short bowel, colectomy
Infections leading to inflammation, injury or loss of absorptive function
Whipple’s, tropical sprue, giardia, small bowel bacterial overgrowth, TB
Parasites (e.g. worms and flukes)
Opportunistic infections e.g. CMV, cryptosporidium
Other Inflammatory conditions – crohn’s, coeliac
Disease in associated digestive organs – acute or chronic pancreatitis, atrophic gastritis, biliary and liver disorders
Malignancy – leading to mucosal injury or loss during therapy
E.g. lymphoma and adenocarcinoma
Other causes of mucosal injury
Radiotherapy, chemotherapy, other common drugs e.g. NSIADS, nicorandil

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17
Q

Malabsorption of key nutrients presentation:
Iron
Folate
B12
Vitamin d
Fat soluble vitamins or fats
Sodium potassium and water balance
Protein energy misbalance
Ca, PO4 and Mg
Selenium, zinc, copper

A

Iron – usually chronic blood loss rather than malabsorption, but may relate to duodenal/jejunal disease

Folate – proximal disease e.g. coeliac, UGI Crohn’s

B12 – pernicious anaemia and ileal issues
Vitamin d – usually multifactorial

Fat soluble vitamins or fats – pancreas, cholestasis, short bowel

Sodium potassium and water balance – colonic disease or loss

Protein energy misbalance – short bowel, or non functioning gut

Ca, PO4 and Mg – tetany, fatigue, myopathy or neuropathy, rarely heart failure

Selenium, zinc, copper – very rare, symptoms including neuropathy, myopathy poor wound healing and cardiac failure

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18
Q

Coeliac disease presentation

A

GI S&S: indigestion, bloating, abdominal pain, CIBH
Non GI S&S: ataxia, skin rash (DH), fatigue, nutrient deficiency – e.g. iron, Vit D
Complications: osteoporosis, malignancy (intestinal lymphoma), anaemia, neuropathy, impaired fertility (F)

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19
Q

Investigations for coeliac

A

Blood test – options
IgA TTG
Add EMA if weak positive
If IgA deficient check IgG EMA
Adults – recommend a biopsy to confirm
Findings – increased IELs, villous atrophy

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20
Q

Crohn’s types and features and (extra intestinal)

A

Types:
Ileo-colitis,
Ileitis,
Oesophago-Gastroduodenitis
Jejunoileitis
Granulomatous Colitis
Perianal Disease

Strictures, fistulas, abscesses
More likely to be malabsorption
Pain more likely on rhs

Macroscopic Features:
Skip Lesions
Cobblestone Appearance
Aphthous and Serpentine Ulcers
Fat stranding

Gall stones
Erythema nodosum

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21
Q

UC types and features

A

Types:
Proctitis
Proctosigmoiditis
Distal Colitis
Extensive Colitis
Pancolitis

loss of haustra, thumbprinting on AXR

Macroscopic Features:
Superficial Ulceration
Pseudo polyp formation
Distal to proximal spread
Backwash Ileitis

Primary sclerosing cholangitis

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22
Q

IBD investigations and findings

A

ESR ( Erythrocyte Sedimentation rate) and CRP( C-reactive Protein)
Raised Systemic inflammatory Markers

Serological markers pANCA (perinuclear Anti Neutrophil Cytoplasmic Antibodies)
Positive

Iron studies, CBC
Anaemia, Raised WCC, Raised platelets

Antigen/Enzyme testing ( Calprotectin, Lactoferrin, Elastase) Raised Intestinal Inflammatory Markers

Culture
C. difficile and other microbes

Plain Abdominal Film, CT or MRI
Thumb printing, bowel wall dilatation, abscess and fistula , fat stranding, Sacroiliitis,

Colonoscopy
Macro- Skip lesions, cobblestone, serpentine ulcers in CD; Ulcerations and Pseudo-polyps in UC
Micro- Transmural/ superficial chronic inflammation

X-ray
String sign in CD (Now not commonly used due to complications)

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23
Q

IBD treatment (first to last resort)

A

Tier 1: 5-ASAs (e.g. mesalazine, sulfasalazine) - generally for ulcerative colitis only

Tier 2: Steroids (e.g. prednisolone, budesonide)

Tier 3: Immunomodulators (e.g. azathioprine, mercaptopurine, methotrexate)

Tier 4: Biologics (e.g. adalimumab, stelara, infliximab)

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24
Q

UC management - moderate and severe (what is severe?) flare, and maintenance.

A

Mild - topical aminosalicylate (mesalazine)- oral if more extensive disease
Oral pred after 4 weeks with no improvement

Severe (bowels >6 times per day with blood, tachycardic, >37.5ºC). Anaemic (Hb <105), CRP >30). - i.v. corticosteroids

Remission - 5-ASAs (mesalazine)
If >2 exacerbations in the past year thiopurines

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25
Q

Crohns management - moderate and severe flare, and maintenance.

A

Mild - oral pred

Severe - i.v. hydrocortisone, parenteral nutrition. Then thiopurines (azathioprine) if needed.

Remission - Thiopurines (azathioprine)
methotrexate 2nd line

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26
Q

C. diff investigations

A

Full blood count
Renal profile
C reactive protein
Lactate

Stool sample
Start with PCR test for C.diff toxin gene (means toxigenic strain of C.diff present)
Then if positive an EIA test to evaluate if the strain present is producing toxins

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27
Q

C. diff toxins

A

B 1000x worse than A

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28
Q

When to do CT in C diff

A

CT abdomen if abdominal pain – the concern is toxic colitis which may lead to perforation

Imaging findings
Dilatation
Loss of haustral markings
Thumbprinting
Thick walls

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29
Q

C diff Flexible sigmoidoscopy findings

A

Pseudomembranes manifest as raised yellow or off-white plaques up to 2 cm in diameter scattered over the colonic mucosa

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30
Q

C. diff treatment

A

Isolate patient, start enteric precautions

2) Start oral vancomycin or fidaxomicin

3) Rationalise current broad spectrum antibiotics

4) If possible, stop proton pump inhibitor treatment

Faecal microbiota transplantation; Used if two or more recurrences of C.diff infection

Iv metronidazole if severe

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31
Q

Diagnosis of Diabetes

A

Symptomatic::
A single fasting plasma glucose ≥ 7.o mmol/l
OR
A single random plasma glucose ≥ 11.1 mmol/l
OR
An HbA1c ≥ 48 mmol/mol (6.5%) *

Asymptomatic:
A fasting glucose ≥ 7.0 on two separate occasions
OR
A random glucose ≥ 11.1 on two separate occasions
OR
A 2 hour plasma glucose>11.1 on OGGT (after 75g glucose)
OR
An HbA1c ≥ 48 mmol/mol (6.5%) on two separate occasions

Impaired fasting glycaemia – plasma glucose 6.1-6.9 mmol/l
Impaired glucose tolerance – 2 hours plasma glucose 7.8-11.0 mmol/l
High risk of diabetes – HbA1c 42-47 mmol/mol

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32
Q

Situations where HbA1c is not appropriate for diagnosis of diabetes:

A

ALL children and young people
Suspected Type 1 diabetes
Symptoms less than 2 months
Acutely ill (e.g. requiring hospital admission)
Medication that may cause rapid glucose rise e.g. steroids, antipsychotics
Acute pancreatic damage, including pancreatic surgery
In pregnancy
Presence of genetic, haematologic and illness-related factors that influence HbA1c and its measurement
CKD 4/5

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33
Q

Metformin:
Action
CV Risk
Hypoglycaemia
Weight
Cost
↓HbA1C
Side-effects
Contra-indications

A

Action: Decreases gluconeogenesis and increases peripheral utilization

CV Risk: Decreases

Hypoglycaemia: Rare

Weight: Loss

Cost: £

↓HbA1C: High

Side-effects: Diarrhoea, vomiting, rarely lactic acidosis

Contra-indications: eGFR <30ml/min, AKI, contrast media, surgery

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34
Q

Gliclazide:
Class
Action
CV Risk
Hypoglycaemia
Weight
↓HbA1C
Side-effects
Contra-indications

A

Sulphonylureas

Action: Enhances the ability of the pancreas to secrete insulin

CV Risk: Uncertain

Hypoglycaemia: Common

Weight: Gain

↓HbA1C: High

Side-effects: Mainly gastrointestinal (GI)

Contra-indications: Avoid long-acting in elderly/renal, acute porphyria, severe hepatic impairment

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35
Q

Pioglitazone
Action
CV Risk
Hypoglycaemia
Weight
↓HbA1C
Side-effects
Contra-indications

A

Thiazolidinediones “Glitazones”:

Action: Reduces peripheral resistance

CV Risk: Insufficient evidence

Hypoglycaemia: Low risk

Weight: Gain

↓HbA1C: High

Side-effects: Increases risk of CHF, oedema, fractures
Contra-indications: CHF, previous or active bladder cancer, uninvestigated macroscopic haematuria

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36
Q

Sitagliptin
Action
CV Risk
Hypoglycaemia
Weight
↓HbA1C
Side-effects
Contra-indications

A

Dipeptidyl Peptidase-4 Inhibitors “Gliptins”:

Action: prevent the breakdown of incretins GLP;Increases insulin secretion and decreases glucagon release

CV Risk: Unknown

Hypoglycaemia: Low risk

Weight: Neutral

↓HbA1C: Moderate

Side-effects: Gastrointestinal oedema, increased risk of infections, acute pancreatitis

Contra-indications: Ketoacidosis

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37
Q

Glucagon-Like Peptide-1 Agonists:
E.g.
Action
CV Risk
Hypoglycaemia
Weight
Cost
↓HbA1C
Side-effects
Contra-indications

A

E.g.: Exenatide

Action: Increases insulin secretion, inhibits inappropriate glucagon secretion, slows gastric emptying, reduces appetite

CV Risk: Liraglutide decreases, rest unknown

Hypoglycaemia: Rare

Weight: Loss

Cost: £££

↓HbA1C: High

Side-effects: Mainly GI, especially nausea, acute pancreatitis
Contra-indications: Ketoacidosis; inflammatory bowel disease; diabetic gastroparesis; pancreatitis

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38
Q

Sodium Glucose Co-Transporter 2 (SGLT2) Inhibitor:
E.g.
Action
CV Risk
Hypoglycaemia
Weight
Cost
↓HbA1C
Side-effects
Contra-indications

A

E.g.: Dapagliflozin

Action: Reversibly inhibits SGLT2 in the renal proximal convoluted tubule to reduce glucose reabsorption and increase urinary glucose excretion

CV Risk: Decreases

Hypoglycaemia: Common

Weight: Loss

Cost: ££

↓HbA1C: Moderate
Side-effects: Constipation, UTIs, dysuria, sweating and thirst. Risk of DKA

Contra-indications: eGFR <60ml/min, ketoacidosis. Caution in elderly or with hypotension

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39
Q

Anti-diabetic drugs more likely to cause hypoglycaemia

A

sulfonylureas (gliclazide)
SGLT2 inhibitors (-flozins)

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40
Q

Causes of death in DKA

A

Cerebral oedema (paediatric, young adults), hypokalaemia, ARDS, co-morbid conditions

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41
Q

DKA pathogenesis

A

Progressive metabolic disturbance due to
Insufficient insulin i.e. type I diabetes
Contributory effects of counter-regulatory hormones

==> Metabolic acidosis

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42
Q

Clinical features of DKA

A

Osmotic symptoms
Weight loss
Breathlessness – Kussmaul resps
Abdo pain – children in particular
Leg cramps
Nausea and vomiting
Confusion
Drowsiness

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43
Q

Diagnosis of DKA

A

All three required
. Raised blood glucose>11mmol /L or known diabetes
. Capillary ketones > 3 mmol/L (or Ketones >2+ in urine)
. Venous pH < 7.3 or venous bicarb < 15mmol/L

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44
Q

Management of DKA

A

IV insulin – fixed rate 0.1 unit/kg/hour
IV fluid replacement: 0.9% NaCL 1L over 1 hour or 500ml over 10 min if sbp <90
IV electrolyte replacement (potassium) if needed

Once blood glucose < 14 mmol/l: 10% dextrose 25 mls/hr in addition to the saline regime

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45
Q

Management of diabetes
1st, 2nd, 3rd line therapy

A

First line: Metformin

Second-line therapy
Dual therapy - add one of the following:
metformin + DPP-4 inhibitor
metformin + pioglitazone
metformin + sulfonylurea
metformin + SGLT-2 inhibitor (if NICE criteria met)

Third-line therapy
If a patient does not achieve control on dual therapy then the following options are possible:
metformin + DPP-4 inhibitor + sulfonylurea
metformin + pioglitazone + sulfonylurea
metformin + (pioglitazone or sulfonylurea or DPP-4 inhibitor) + SGLT-2 if certain NICE criteria are met
insulin-based treatment

Further therapy

If triple therapy is not effective or tolerated consider switching one of the drugs for a GLP-1 mimetic:
BMI ≥ 35 kg/m² and specific psychological or other medical problems associated with obesity or
BMI < 35 kg/m² and for whom insulin therapy would have significant occupational implications or weight loss would benefit other significant obesity-related comorbidities
only continue if there is a reduction of at least 11 mmol/mol [1.0%] in HbA1c and a weight loss of at least 3% of initial body weight in 6 months

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46
Q

Hyperosmolar hyperglycaemic state diagnosis

A

Hypovolaemia
hyperglycaemic >30mmol/L without ketones
Osmolality >320 mosmol/kg

(2 (Na) + glucose + urea
> 340 mOsm/kg associated with impairment of consciousness)

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47
Q

Clinical features of HHS

A

Symptoms/signs of intercurrent infection
Severe dehydration
CNS presentation common; Seizures, Aphasia, Hemianopia, Unilateral hyperreflexia, Extensor babinski, Myoclonic jerks, Nystagmus

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48
Q

Complications of HHS

A

Vascular complications:
MI
CVA
Arterial thrombosis

Other complications:
Seizures
Cerebral oedema
Osmotic demyelination
At risk of foot complications

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49
Q

HHS management

A

1L 0.9% NaCl over one hour
3-6L over 24 hours
+- Potassium

Low dose i.v. insulin once fall in glucose is <5mmol/L/hr

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50
Q

Hypoglycaemia symptoms

A

Acutely unwell
Drowsy
Agitated
Unconscious
Fitting/Seizures

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51
Q

Causes of hypoglycaemia in hospital

A

Missed meals
Reduced appetite
Nil by mouth
AKI (insulin is renally secreted)
Prescription errors: doses, timing, type of insulin

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52
Q

Treatment of hypoglycaemia in patients co-operative and able to swallow

A

Give 15-20g quick acting carbs; (60mls/ 1 bottle Glucojuice/LIFT, 2 tubes glucose gel, Patient’s usual hypo treatment)

Once glucose > 4.0, give long-acting Carbs

Repeat CBG after 10-15 minutes.
Treatment can be repeated up to 3 times.

If still low, give i.v. glucose

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53
Q

Treatment of hypoglycaemia in patients unconscious/aggressive/un-cooperative

A

Glucagon 1mg IM (Takes ~ 15 min to act; Less effective in;
malnourished
those with prolonged starvation
severe liver disease
alcohol intake)

100mls 20% glucose over 15 minutes IV if access already done

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54
Q

Neuropathy complications from chronic hyperglycaemia:

Retinopathy
Nephropathy
Neuropathy
Macrovascular

A

Retinopathy
Background
Pre-proliferative
Proliferative
Maculopathy
Nephropathy

Neuropathy
nephrotic syndromes

Peripheral neuropathy
Classic glove and stocking distribution
Often painful – NICE guidance for treatment
Neuropathic foot ulceration/Charcot joints

Autonomic neuropathy
Postural hypotension
Tachycardia
Bowel and bladder dysfunction
Gastroparesis
Erectile dysfunction
Sweating- gustatory, anhidrosis

Others
Mononeuropathy e.g III or VI nerve palsies
Radiculopathy
Diabetic amyotrophy

Cerebrovascular disease
Ischaemic heart disease, hypertension
Peripheral vascular disease

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55
Q

MEN SYNDROME

A

MEN 1 - Pituitary adenoma, parathyroid hyperplasia, pancreatic tumours

MEN 2A - Parathyroid hyperplasia, medullary thyroid carcinoma, phaeochromocytoma

MEN 2B - Mucosal neuroma, marfanoid appearance, medullary thyroid carcinoma, phaeochromocytoma

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56
Q

Hypothyroidism

A

Thyroxine tablets
1.6 mcg/kg body weight
Then titre to give sufficient to suppress TSH to normal

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57
Q

Causes of diffuse, multinodular and solitary nodule goitres

A

Diffuse
Graves’ disease
Hashimoto’s

Multinodular goitre
Chronic iodine deficiency; Thyroid gland stimulated by TSH over years; Usually normal thyroid function

Solitary nodule
Cyst
Adenoma
Carcinoma

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58
Q

Treatment of hyperthyroid

A

Thyroidectomy
Carbimazole/ propylthiouracil (used in pregnancy)
RAI

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59
Q

Treatment of subclinical hypothyroidism

A

TSH is > 10mU/L and the free thyroxine level is within the normal range
consider offering levothyroxine if the TSH level is > 10 mU/L on 2 separate occasions 3 months apart

TSH is between 5.5 - 10mU/L and the free thyroxine level is within the normal range
if < 65 years consider offering a 6-month trial of levothyroxine if:
the TSH level is 5.5 - 10mU/L on 2 separate occasions 3 months apart,and
there are symptoms of hypothyroidism
in older people (especially those aged over 80 years) follow a ‘watch and wait’ strategy is often used
if asymptomatic people, observe and repeat thyroid function in 6 months

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60
Q

Acute thyroiditis management

A

Propranolol for toxic stage and analgesia

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61
Q

Myxoedemic coma and treatment

A

E.g. On examination, she is found to be hypothermic, hypotensive, and bradycardic. Her skin is very dry and flaky. Her BMI is 32 kg/m2. She has bilateral non-pitting oedema and thinning hair.

IV thyroxine and hydrocortisone

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62
Q

Types of thyroid cancer

A

Papillary good prog
Follicular good prog
Medullary good prog
Anaplastic bad prog

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63
Q

Toxic multinodular goitre and treatment

A

Toxic multinodular goitre describes a thyroid gland that contains a number of autonomously functioning thyroid nodules resulting in hyperthyroidism.

The treatment of choice is radioiodine therapy.

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64
Q

Causes of Secondary Hypertension

A

Cushing’s
Conn’s
Thyroid dysfunction
Acromegaly
Phaeochromocytoma
Hyperparathyroidism

Renal disease

Coarctation of aorta
Obstructive Sleep Apnoea

Alcohol
Cocaine
COCP
Anti-depressant
Herbal remedies

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65
Q

Malignant Hypertension

A

> 180/120
+ End organ damage (eg. cerebral haemorrhage, acute renal failure, aortic dissection or heart failure)
Must have signs of papilloedema to make a diagnosis of malignant hypertension

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66
Q

Hypertensive retinopathy
-4 grades

A

I Tortuous arteries with shiny walls (copper/silver wiring)

II A-V nipping – narrowing as arterioles cross veins

III Flame haemorrhages and cotton wool spots

IV Papilloedema

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67
Q

Hypertensive Arteriosclerosis histology

A

Hypertrophy of media

Fibroelastic thickening of intima

Elastic lamina reduplication

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68
Q

HYPERTENSIVE Arteriolosclerosis histology

A

Replacement of wall structures by amorphous hyaline material

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69
Q

Mycotic aneurysm

A

Mostly caused by endocarditis (infection of heart valve)
Bacterial septicaemia
Infection of arterial wall

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70
Q

CCS grading of chest pain

A

I Angina only with strenuous exertion Presence of angina during strenuous, rapid, or prolonged ordinary activity (walking or climbing the stairs).

II Angina with moderate exertion Slight limitation of ordinary activities when they are performed rapidly, after meals, in cold, in wind, under emotional stress, during the first few hours after waking up, but also walking uphill, climbing more than one flight of ordinary stairs at a normal pace and in normal conditions.

III Angina with mild exertion Having difficulties walking one or two blocks or climbing one flight of stairs at normal
pace and conditions.

IV Angina at rest No exertion needed to trigger angina.

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71
Q

Stable angina investigations

A

ECG, Bloods, CXR, echo
CTCA Gold standard

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72
Q

Stable angina management

A

S/L GTN for all
Betablocker first line (HR 55-60bpm) / calcium channel blocker if not tolerated
Aspirin
Statin

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73
Q

Which vessels can be used in CABG

A

Internal mammary artery
saphenous vein
radial artery

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74
Q

3 types of acute coronary syndrome

A

Unstable angina
NSTEMI
STEMI

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75
Q

Differentials for ACS

A

Peri/Myocarditis
Coronary artery spasm
Tako Tsubo cardiomyopathy
Aortic dissection
Pulmonary embolism
Pneumothorax/pleurisy
Musculo-skeletal/PUD/Chostochondirits, oesophagitis, herpes zoster

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76
Q

Acute and longer term management of STEMI

A

3oomg aspirin, i.v. morphine, o2, i.v. nitrates

PCI within 90 minutes (Give DAPT + unfractionated heparin + Gpiib/iiia inhibitor

If not, fibrinolysis (fondaparinux given before)

If fibrinolysis fails and ECG STEMI after 90mins: urgent PCI

Long term:
Aspirin 75mg + clopidogrel
ACEI
Statin
B Blocker

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77
Q

Mesothelioma diagnosis test

A

histology, following a thoracoscopy

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78
Q

NSTEMI/UA management

A

GRACE score
NSTEMI management: patients with a GRACE score > 3% should have coronary angiography within 72 hours of admission
Semielective PCI

B – Base the decision about angiography and PCI on the GRACE score
A – Aspirin 300mg stat dose
T – Ticagrelor 180mg stat dose (clopidogrel if high bleeding risk, or prasugrel if having angiography)
M – Morphine titrated to control pain
A – Antithrombin therapy with fondaparinux (unless high bleeding risk or immediate angiography)
N – Nitrate (GTN)

If PCI: unfractionated heparin should be given
further antiplatelet (‘dual antiplatelet therapy’, i.e. aspirin + another drug) prior to PCI
if the patient is not taking an oral anticoagulant: prasugrel or ticagrelor
if taking an oral anticoagulant: clopidogrel

Conservative management for patients with NSTEMI/unstable angina
if the patient is not at a high risk of bleeding: ticagrelor
if the patient is at a high risk of bleeding: clopidogrel

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79
Q

ACS complications

A

Early:
Free wall rupture
Pulmonary oedema
Cardiogenic shock
VSD
Mitral regurg; ruptured chordae tendinae
LV aneurysm
Rhythm disturbance; VE, NSVT, VF, SVT, Brady-arrhythmias

Late:
DVT (early ambulation or VTE prophylaxis)
LV thrombus
Pericarditis (Dressler’s)

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80
Q

Dressler’s syndrome

A

Immune medicated pericarditis
Increased ESR and anti-myocardial antibodies
Different kind of chest pain
Give high dose aspirin/NSAIDs

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81
Q

Causes of Elevated Troponins

A

Cardiac Causes Non-cardiac diseases
Cardiac amyloidosis Critically ill patients
Cardiac contusion High dose chemotherapy
Cardiac surgery Primary pulmonary hypertension
Cardioversion and implantable Pulmonary embolism
cardioverter defibrillator shocks Renal failure
Closure of atrial septal defects Subarachnoid haemorrhage
Coronary vasospasm Scorpion envenoming
Dilated cardiomyopathy Sepsis and septic shock
Heart failure Stroke
Hypertrophic cardiomyopathy Ultra-endurance exercise
Myocarditis
Percutaneous coronary intervention
Post cardiac transplantation
Radiofrequency ablation
Supraventricular tachycardia

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82
Q

Driving restrictions cardiac disease/events (DVLA)

A

Angina – can drive when symptoms controlled
ACS – 1 week if PCI and LVEF>40% and no planned revasc in next 4 weeks. Otherwise 1 month
CABG – 4 weeks
ICD – 6 months
CHF – Cannot drive if NYHA IV
Arrhythmia- 4 weeks controlled

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83
Q

Tako Tsubo cardiomyopathy

A

“Broken Heart syndrome”
90% post-menopausal females
Extreme physical/emotional stress/grief
Chest pain, sweating, breathlessness
ECG changes suggesting a STEMI
Normal coronary arteries on angiogram.

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84
Q

QRS direction in different lead

A

Positive in I, II, V4-V6
Negative in aVR, V1 and V2

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85
Q

QT interval normal duration

A

Males: <0.40 secs (2 big squares)
Females: <0.44 secs (11 small, or 2 big 1 small)

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86
Q

Cardiac axis

A

In normal axis, the axis is towards both Lead I and aVF, so the QRS complexes will both appear to point upwards

In left axis deviation, the axis is towards Lead I (so QRS will point up), but away from aVF (so QRS will point down)

In right axis deviation, the axis is away from Lead I (so QRS will point down), but towards aVF (so QRS will point up)

In extreme axis, the axis is away from both Lead I and aVF, so the QRS complexes will both appear to point downwards

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87
Q

“Tall and Tented” T wave

A

“Tall and Tented”?
Tall:
At least ½ the amplitude of the preceding QRS complex)
Tented:
Look as if they’ve been pinched from above - i.e. a pointed peak, narrow base

Hyperkalaemia

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88
Q

Normal T wave inversion

A

This can be a normal variant in Leads V1 and III

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89
Q

Which heart blocks require pacing

A

1st degree & 2nd degree (Mobitz I) heart blocks tend to be asymptomatic, and don’t tend to require pacing

2nd degree (Mobitz II) & 3rd degree heart blocks carry a high risk of asystole, and require pacemaker implantation

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90
Q

Delta Wave on the ECG

A

Accessory Pathways - typical of Wolff-parkinson-white

Early depolarisation of part of the ventricle (seen as a Delta Wave on the ECG), however the action potential propagates slowly, as it spreads cell-to-cell through the heart muscle

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91
Q

STEMI - Chronic ECG Changes

A

At onset of pain - the ECG shows a normal sinus complex
Within 1 hour - noticeable ST segment elevation has developed
Following treatment - subsequently, T-wave inversion may develop
24h later - ST segment has returned to baseline, T-wave inversion persists
Days/Months later - deep Q-wave indicating tissue death

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92
Q

Tombstoning on ECG

A

proximal LAD occlusion with poor LV ejection fraction

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93
Q

S1Q3T3 pattern

A

“classic” for PE, but rare:
Deep S-wave (Lead I)
Q wave (Lead III)
Inverted T-wave (Lead III)

94
Q

LBBB ECG

A

Dominant S wave in V1
Broad monophasic R wave in lateral leads (I, aVL, V5-6)
Absence of Q waves in lateral leads
Prolonged R wave peak time > 60ms in leads V5-6

WiLLiaM

95
Q

RBBB ECG

A

RSR’ pattern in V1-3 (“M-shaped” QRS complex)
Wide, slurred S wave in lateral leads (I, aVL, V5-6)

MaRRoW

96
Q

Classification of AF

A

Paroxysmal
Self-terminates usually within 48 hours
Persistent
AF lasting >7 days or requires termination with cardioversion (Chemical or electrical)
Permanent
Both patient and physician accept the presence of AF; Rhythm control interventions are not pursued.

97
Q

CHA2DS2VASc

A

C: Congestive heart failure (1 point)
H: Hypertension (1 point)
A₂: Age ≥75 years (2 points)
D: Diabetes mellitus (1 point)
S₂: Prior Stroke or transient ischemic attack (TIA) or thromboembolism (2 points)
V: Vascular disease (such as previous myocardial infarction, peripheral artery disease, or aortic plaque) (1 point)
A: Age 65-74 years (1 point)
Sc: Sex category (Female sex) (1 point)

CHA2DS2VASc 0 No anticoagulation
CHA2DS2VASc 1 Male - Consider OAC
CHA2DS2VASc 2 Recommend OAC

98
Q

Mechanical valve or moderate to severe mitral stenosis Thrombo-embolic prophylaxis

A

VKA

99
Q

What Thrombo-embolic prophylaxis is used in AF

A

DOAC or warfarin (if valvular)

100
Q

Rate control in AF

A

Initial monotherapy with standard β-blocker or rate-limiting CCB (assuming LVEF >40%)

Digoxin monotherapy only for non-paroxysmal AF in sedentary patients

If monotherapy does not control symptoms, combine 2 of:
β-blocker
Diltiazem
Digoxin

101
Q

Rate control in non-paroxysmal AF sedentary pt

A

Digoxin monotherapy only for non-paroxysmal AF in sedentary patients

102
Q

Management of acute onset AF

A

Unstable – DCC
Stable, onset <48 hours – DCC

or
Flecainide/propafenone if no cvd
Amiodarone if impaired LV
Amiodarone/Sotalol if known CAD or Structural Heart Disease
Used if underlying cause

103
Q

Ablation for AF

A

Pulmonary vein isolation
+ Posterior wall of LA
Radiofrequency energy or cryoablation
Usually second line to antiarrhythmic drugs
First line in selected patients
A Flutter ablation high success rate (90+%)
PAF success rates 70-75%
Persistent AF success rates 50-60%

104
Q

Bradycardia treatment

A

If pt has adverse signs:
500ug atropine; repeated up to 3mg if needed
+- External pacing

105
Q

SVT treatment

A

DCC if pt unstable

Vagal manoeuvres - carotid sinus massage/ valsalva manoeuvre
Adenosine 6mg then 12mg then 12mg
Then DCC

106
Q

VT treatment

A

DCC if pt unstable; Emergency defib
After 3 shocks 1mg i.v. adrenaline and
amiodarone 300 mg IV approximately every 3 - 5 min

Amiodarone

107
Q

VF treatment

A

Emergency defib
After 3 shocks 1mg i.v. adrenaline (0.5ml 1:1000) and
amiodarone 300 mg IV approximately every 3 - 5 min

108
Q

Levels of Severity of Acute Asthma Attacks in Adults

A

Moderate Asthma:
Increasing symptoms.
Peak Expiratory Flow (PEF): >50-75% of best or predicted.
No features of acute severe asthma.

Acute Severe Asthma:
Criteria: Any one of the following:
PEF 33-50% of best or predicted.
Respiratory rate ≥25/min.
Heart rate ≥110/min.
Inability to complete sentences in one breath.

Life-Threatening Asthma: Any one of the following
Altered conscious level.
Exhaustion.
Arrhythmia.
Hypotension.
Cyanosis.
Silent chest.
Poor respiratory effort.
PEF <33% of best or predicted.
SpO2 <92%.
PaO2 <8 kPa.
‘Normal’ PaCO2 (4.6-6.0 kPa).

Near-Fatal Asthma
Criteria: Raised PaCO2 and/or requiring mechanical ventilation with raised inflation pressures.

109
Q

Management of acute asthma

A

IMMEDIATE TREATMENT
Oxygen to maintain SpO₂ 94-98%
β₂ bronchodilator (salbutamol 5 mg) via an oxygen-driven nebuliser
Ipratropium bromide 0.5 mg via an oxygen-driven nebuliser
Prednisolone tablets 40-50 mg or IV hydrocortisone 100 mg
No sedatives of any kind
Chest X-ray if pneumothorax or consolidation are suspected or patient requires mechanical ventilation

IF LIFE-THREATENING FEATURES ARE PRESENT:
Discuss with senior clinician and ICU team
Consider IV magnesium sulphate 1.2-2 g infusion over 20 minutes (unless already given)
Give nebulised β₂ bronchodilator more frequently, e.g., salbutamol 5 mg up to every 15-30 minutes or 10 mg per hour via continuous nebulisation (requires special nebuliser)

SUBSEQUENT MANAGEMENT
IF PATIENT IS IMPROVING continue:
Oxygen to maintain SpO₂ 94-98%
Prednisolone 40-50 mg daily or IV hydrocortisone 100 mg 6 hourly
Nebulised β₂ bronchodilator with ipratropium 4-6 hourly
IF PATIENT NOT IMPROVING AFTER 15-30 MINUTES:
Continue oxygen and steroids
Use continuous nebulisation of salbutamol at 5-10 mg/hour if an appropriate nebuliser is available. Otherwise, give nebulised salbutamol 5 mg every 15-30 minutes
Continue ipratropium 0.5 mg 4-6 hourly until patient is improving
IF PATIENT IS STILL NOT IMPROVING:
Discuss patient with senior clinician and ICU team
Consider IV magnesium sulphate 1.2-2 g over 20 minutes (unless already given)
Senior clinician may consider use of IV β₂ bronchodilator or IV aminophylline or progression to mechanical ventilation

110
Q

Discharging acute asthma pt

A

Be on discharge medication for 24 hours
PEF >75%
Oral and inhaled steroids + bronchodilators

111
Q

COPD exacerbation management

A

SABA
30mg oral pred 7 days
+- abx
02 if needed

112
Q

COPD long term management

A

SABA or SAMA
Inhaled corticosteriod
LABA or LAMA
Rescue medication

phosphodiesterase-4 (PDE-4) inhibitor if many exacerbations

113
Q

COPD severity classes

A

Uses FEV1
Mild >80%
Moderate 50-80%
Severe 30-50%
Very severe <30%

114
Q

Prophylaxis in COPD

A

NICE guidelines suggest a prescription of 250mg azithromycin three times per week if:
The patient no longer smokes.
Has optimised non-pharmacological management & inhaled therapies.
Referred to pulmonary rehab (if appropriate).
4 acute exacerbations in the last year (producing sputum), requiring hospital admission at least once.

115
Q

Long Term Oxygen Therapy criteria

A

pO2 <7.3 kPa when stable
pO2 <8kPa plus polycythaemia or cor pulmonale

116
Q

Acute COPD exacerbation management if all standard medications fail

A

NIV should be considered in all patients with an acute exacerbation of COPD in whom a respiratory acidosis (PaCO2>6kPa, pH 7.35-7.26) persists despite immediate maximum standard medical treatment

117
Q

ABG indications for ventilation

A

NIV: Type II resp failure - COPD, Obesity, chest wall disorder, neuromuscular

Invasive Type I and II

118
Q

Bronchiectasis on CT

A

Signet ring

119
Q

Bronchiectasis on examination

A

Clubbing
Coarse crackles
RHF
inspiratory squeaks
expiratory wheeze

120
Q

Most common bronchiectasis inf. pathogens

A

Haem influenza
s pneumoniae
pseudomonas

121
Q

Active TB management and ADRs of those drugs

A

6 months: Isoniazid (with pyridoxine) + rifampicin
pyrazinamide +ethambutol for first 2 months too

Rifampicin - deranged LFTs, pink urine
Isoniazid - peripheral neuropathy pyridoxine should prevent this
pyrazinamide - hepatotoxic
ethambutol - optic neuritis

122
Q

Latent TB management and ADRs of those drugs

A

3 months Isoniazid (with pyridoxine) + rifampicin

Rifampicin - deranged LFTs, pink urine
Isoniazid - peripheral neuropathy pyridoxine should prevent this

123
Q

TB mantoux test results

A

positive if:
5mm: previous exposure
10mm: risk factors
15mm: anyt indivual

124
Q

Lung cancer types, regions and typical pt

A

Smoking and central lung - small cell, squamous
Peripheral - adenocarcinoma (increased in asbestosis), large cell

125
Q

Paraneoplastic syndromes

A

Small cell
ADH - SIADH -> hyponatraemia
ACTH; Cushings
Lambert Eaton syndrome; myasthenia like sx.

Squamous
rPTH; Hypercalcaemia

126
Q

Clinical signs (not sx) of Lung ca

A

Clubbing
Hypertrophic pulmonary osteoarthropathy; inflamm of small joints in hand

127
Q

Complications of lung ca

A

Recurrent laryngeal nerve palsy
Phrenic nerve palsy
SVC obstruction
Pancoast syndrome

128
Q

Causes of ILD

A

Idiopathic
Occupation
Nitrofurantoin, amiodarone, sulfalazine, methotrexate
extrinsic allergic alveolitis
TB, Fungal, viral
Sarcoidosis, RA, SLE, scleroderma

129
Q

ILD on CT

A

Honeycombing

130
Q

Hypersensitivity pneumonitis (HP) acute and chronic

A

Exposure to inhaled organic antigen to which the person has been previously sensitised
Acute HP – short period of intense exposure, usually reversible; Type III hypersensitivity
Chronic HP – long-term lower level exposure, less reversible and may progress; type IV hypersensitivity

131
Q

Acute management of Hypersensitivity pneumonitis

A

O2 and oral pred

132
Q

Hypersensitivity pneumonitis diagnosis

A

Thorough history!
Bloods (precipitins)
Imaging
Lung function testing
BAL / biopsy?
MDT

133
Q

Simple vs massive coal workers pneumoconiosis

A

Simple coal worker’s pneumoconiosis = bilateral nodules
Risk of Progressive massive fibrosis (PMF) if exposure continues

134
Q

Asbestos related lung disease

A

Pleural plaques
Benign
Thickened calcified areas on pleura
Not pre-malignant / don’t progress – indicate exposure

Thickening
Can get benign effusions, rounded atelectasis, diffuse pleural thickening.
May have symptoms eg SOB, restrictive spiro – so may get compensation.

Asbestosis looks like IPF – interstitial lung disease

Mesothelioma = malignant tumour of pleura

135
Q

CURB65 score

A

Confusion- AMT ≤ 8/10 or disorientated in time, place or person
Urea > 7 mmol/L
Respiratory Rate ≥ 30/ min
Blood Pressure- systolic BP < 90mmHg +/- diastolic BP < 60mmHg

Age over 65 years

0 - PO amoxicillin at home
1-2 oral/i.v. amox and clarithro
3+ i.v. co-amox and clarithro

136
Q

HAP management and pathogens

A

Mild - oral doxy
Severe - i.v. tazocin

Gram negative enterobacteria
2. Methicillin-resistant staphylococcus aureus (MRSA)
3. Pseudomonas
4. Klebsiella

137
Q

Upper and lower zone fibrosis diseases

A

Upper zone fibrosis = CHARTS Lower zone fibrosis = RASIO

Coal-worker pneumoconiosis

Histiocytosis-X

Ankylosing spondylitis

Radiation (e.g. for breast cancer)

Tuberculosis

Sarcoidosis and silicosis

Lower
Rheumatoid arthritis

Asbestosis

SLE, scleroderma and Sjogren’s syndrome

Idiopathic pulmonary fibrosis

Others (including drugs)

138
Q

Classes of HF

A

Systolic dysfunction: (HFrEF)
EF<40%
-This means insufficient pumping action
Or impaired contraction.
-This occurs when the ejection fraction is low.

Causes:
Ischemic heart disease
Chronic hypertension
Dilated cardiomyopathy
Myocarditis

Diastolic dysfunction: (HFpEF)
-insufficient filling of the ventricle due to decreased compliance and impaired relaxation.
causes:
Hypertension with left ventricular hypertrophy (LVH)
Restrictive Cardiomyopathy
Hypertrophic Cardiomyopathy
Fibrosis
Amyloidosis
Sarcoidosis
Constrictive pericarditis
Hemochromatosis
Aging

139
Q

Clinical Signs of heart failure l vs r

A

Signs of left sided heart failure:
Crackles in lung bases initially then throughout lung field if left untreated.
Gallop rhythm (an abnormal heart rhythm marked by the occurrence of three distinct sounds in each heartbeat like the sound of agallopinghorse.)
Laterally displaced apex beat
Signs of Right sided heart failure:

Signs of Right sided heart failure:
Remember that in right sided heart failure the blood backed up will cause swelling to the veins, interstitial space and organs.
- Lower limb and sacral pitting edema
- Raised Jugular Venous pressure (JVP)
- Organomegaly (Liver and spleen)
- Ascites

140
Q

NYHA

A

I no limitation
II SOB on exertion
III SOB on normal activity
IV SOB at rest

141
Q

Management of acute heart failure

A

Sit the patient up!
High flow oxygen
IV diuretics (furosemide) at escalating doses
Consider IV nitrates (caution in hypotension and heart failure secondary to severe aortic stenosis!)
(Consider iv opiates and antiemetics)
Consider non-invasive ventilation (CPAP)
Consider inotropic support
Consider device therapy (intra-aortic balloon pump/Impella device)
Consider referral for Left Ventricular Assist Device (Bridge or destination therapy) or Cardiac transplantation

142
Q

Management of chronic heart failure
+ when devices might be indicated

A

Diuretics for symptoms
Ace Inhibitors
Betablockers - stop in pulmonary oedema
Mineralocorticoid Receptor Antagonists (MRA)
Ivabridine to keep HR low
ARNI (Entresto)
Isosorbide mononitrate and dinitrate/Hydralazine (if cannot take ACE i or ARB)
Consideration of CRT if wide QRS >150 milliseconds or /ICD if between 120 and 149 milliseconds

143
Q

ABG for acute HF

A

Initial type I resp failure then type II

144
Q

Mitral stenosis signs and cause and treatment

A

Rheumatic fever
Malar flush, small volume pulse, JVP raised, RV hypertrophy
Mid diastolic with opening snap
Balloon valvuloplasty or replacement

145
Q

Mitral regurgitation signs and cause

A

Post MI, Rheumatic fever, LVH
Systolic thrill
Pansystolic murmur, soft S1; can have 3rd sound
Valve replacement

146
Q

Aortic stenosis signs and cause

A

Calcification of congenital bicuspid valve, rheumatic fever, senile calcific degeneration
Small slow rising pulse, narrow pulse pressure, systolic thrill
Ejection systolic with crescendo, soft s2
Balloon valvuloplasty or replacement

147
Q

Aortic regurgitation signs and cause

A

Post inflamm scarring, infective endocarditis, age, aortic root dilation
Collapsing pulse, wide pulse pressure
Quinckes sign, De musset dign (head nodding with pulse), Pistol shot femorals
Early diastolic murmur, decrescendo
valve replacement

148
Q

Infective endocarditis RF

A

Damaged endocardium
Damaged valves
Prosthetic valves
Congenital heart disease

High levels of sustained bacteraemia
IVDUs
Infected intravascular devices
Untreated abscess/collection elsewhere
Surgery

149
Q

Infective endocarditis def

A

An infectious vegetation on a heart valve

“Pyrexia with a new or changing murmur”

150
Q

Infective endocarditis pathogens and who gets what

A

Streptococcus viridans - most common
Streptococcus mitis
Staphylococcus aureus - IVDUs (now the most most common)
Staph epidermidis - Prosthetic valves (within 2 months)
Streptococcus bovis – found in association with bowel malignancy
Enterococcus – has there been manipulation of GU or GI tract?

‘Culture negative endocarditis’ – difficult to grow organisms
Coxiella burnetii
Bartonella
Brucella
HACEK group:Haemophilus, Actinobacillus, Cardiobacterium, Eikenella, Kingella)

Non infectious endocarditis - systemic lupus erythematosus (Libman-Sacks) lesions

151
Q

Clinical signs of infective endocarditis

A

Murmur
Anaemia
Janeway lesions
Osler’s nodes
Roth’s spots

Pyrexia
Emboli
Nail haemorrhages (splinter haemorrhages)

Splenomegaly
Clubbing

152
Q

Infective endocarditis diagnosis

A

Diagnosis – Dukes criteria

Major Criteria
Typical organism from 2 x separate or persistently +ve typical BCs
Echo findings

Minor criteria
Predisposition (heart condition, IVDU)
Fever >38 degrees C
Vascular phenomena
Immunologic phenomena (Roth spots, glomerulonephritis)
Positive BC (but not meeting major criterion)

2 major and 1 minor criteria
1 major and 3 minor criteria
5 minor criteria

153
Q

Infective endocarditis treatment

A

Medical
Antibiotics (correct choice, strength, frequency and duration)
Empirical choice depends on prosthetic vs. native valve and clinical condition
BSAC (British Society for Antimicrobial Chemotherapy) guidelines

Surgical
Excision of infected or damaged valve and replacement with prosthetic (ideally once not bacteraemic)
Draining of metastatic abscesses

Social
Manage any predisposing factors (eg. IVDU)

154
Q

Transudate vs exudate

A

<30 g/L is a transudate
>30 g/L in an exudate

Lights criteria
The ratio of pleural fluid to serum protein is greater than 0.5
The ratio of pleural fluid to serum LDH is greater than 0.6
The pleural fluid LDH value is greater than two-thirds of the upper limit of the normal serum value

Transudate:
congestive heart failure, liver cirrhosis, nephrotic syndrome

Exudate:
malignancy, infection, pulmonary embolus

155
Q

Pneumothorax treatment

A

Asymptomatic;
primary: regular review as an outpatient
secondary: inpatient admission for monitoring

symptomatic;
High risk: chest drain
Low risk but >2cm aspiration

156
Q

Tension pneumothorax treatment

A

100% O2
large bore cannula into 2nd ICS midclavicular line
Chest drain

157
Q

RF for DVT/PE

A

Hypercoagulable state
Oestrogen therapy (including HRT, COC)
Pregnancy and puerperium (6 weeks post-birth)
Sepsis (and severe infections)
Malignancy
Congestive heart disease
Thrombophilia (inherited):
Factor V Leiden (most common- affects 5% of white Europeans)
Antiphospholipid/lupus anticoagulant (autoimmune)

Stasis
Age (older more at risk)
Venous insufficiency or varicose veins
Obesity (BMI >30)
Immobility (>3 days bed rest)
Continuous travel (e.g. 3h flight or car journey in past 4 weeks)
Hospitalisation

Vessel wall injury
Trauma or surgery (particularly to
lower limbs)
Indwelling venous catheters (e.g. central line)

Additional risk factors
Previous history of VTE
Family history of VTE

158
Q

Wells score for DVT

A

Localized tenderness along the deep venous system +1
Entire leg swollen +1
Calf swelling >3cm compared to other leg (both measured at 10cm distal to tibial tuberosity) +1
Collateral (non-varicose) superficial veins present (on affected leg) +1
Pitting oedema confined to symptomatic leg +1
Active cancer (treatment or palliation within 6 months) +1
Recent bedrest >3 days or major surgery in past 12 weeks +1
Paralysis, paresis or recent immobilised lower extremity (e.g. leg in plaster cast) +1
Previous diagnosis of DVT +1
Alternative diagnosis to DVT as likely or more likely (e.g. trauma) -2

0 -> D-dimer -> US
1-2 -> high sensitivity D-dimer -> US
3+ -> US

159
Q

May-Thurner syndrome

A

Compression of the left common iliac vein by the right common iliac artery causes a DVT to form.

160
Q

PE clinical signs

A

Tachypnoea (increased respiratory rate)
Tachycardia (increased heart rate)
Reduced consciousness (GCS or AVPU)
Hypoxia (low O₂ saturations)
Hypotension (shock)

Dyspnoea 51% (may present as tachypnoea
Pleuritic chest pain 28%
Signs of deep vein thrombosis 18%

161
Q

Wells score for PE

A

Clinical signs and symptoms of DVT (minimum of leg swelling and pain with palpation of the deep veins) +3
Heart rate more than 100 beats per minute +1.5
Haemoptysis +1
Immobilisation for more than 3 days or surgery in the previous 4 weeks +1.5
Previous DVT/PE +1.5
Malignancy (on treatment, treated in the last 6 months, or palliative) +1
There is no diagnosis more likely than PE +3

<4 -> D-dimer then CTPA
>4 -> CTPA with DOAC

If the CTPA is negative then consider a proximal leg vein ultrasound scan if DVT is suspected and ECG

162
Q

Electrocardiogram (ECG) in PE

A

ECG changes are not specific or sensitive enough to diagnose PE.

The ECG may be completely normal (20-25% of patients).
Where there is an abnormality: sinus tachycardia is most common finding.

Other changes:
A dominant R wave in lead V1
T wave inversion in leads V1 –V4 or right bundle branch block
The ‘classical’ ECG finding of a deep, slurred S wave in lead I with a Q wave and T wave inversion in III (S1 Q3 T3 ) is rare in PE- this indicates cor pulmonale.

163
Q

Types of PE

A

Massive (5%) - (Large or extensive
thrombus; saddle; bilateral)
Acute PE with sustained hypotension (systolic BP <90 mmHg or decrease in baseline SBP of 40mmHg or more for more than 15 min or persistent bradycardia <40 bpm)
Mortality > 50% at 90 days

Sub-massive (40%) - (Larger thrombus or embolus than low risk; right heart strained)
Acute PE without hypotension
Signs of right ventricular (RV) dysfunction or myocardial necrosis including:
Abnormalities on echocardiography (see notes)
ECG changes: RV strain, ischemic changes, S1 Q3 T3 pattern
Elevated troponins: why do you think this happens?
Mortality estimated at 16%–22% at 90 days

Low risk (55%) - Smaller emboli
Acute PE without the clinical markers that define massive or sub-massive pulmonary embolism
Mortality estimated at 15% at 90 days

164
Q

PE management

A

Anticoagulation (oral or parenteral) in low risk cases.
3 months if provoked/6 months if unprovoked
Thrombolysis (in patients with haemodynamic compromise) by IV infusion- high risk of bleeding.

165
Q

Causes of reduced erythropoiesis

A

Haematinic deficiency
Iron, folate, B12

  1. Bone marrow disorders
    Infiltration: Myeloma, leukaemia, lymphoma, myelofibrosis, metastatic cancer
    Myelodysplasia
    Aplastic anaemia
  2. Myelosuppressive drugs
    Chemotherapy, co-trimoxazole, multiple others
  3. CKD
    Reduced EPO
  4. Chronic disease/inflammation
    Infection, liver disease, autoimmune inflammatory disorders
  5. Endocrine dysfunction
    Hypothyroid, reduced testosterone
166
Q

iron deficiency anaemia - cause, features, treatment

A

Inadequate intake
Increased requirements, e.g. pregnancy
Malabsorption, e.g. coeliac, gastrectomy
Chronic haemorrhage – e.g. menorrhagia, GI tract

MCV low, Ferritin – roughly correlates with the amount of iron stored in tissues

Oral iron
Suggest a trial of iron if ferritin <25 and/or TF saturation <20
Ferrous Sulphate 200mg = 65mg iron
Ferrous fumurate 210mg = 68mg iron
Ferrous gluconate 300mg = 35mg iron
Expect 10g/l Hb rise every 1-2 weeks if bleeding stopped
Continue at least 3 months to replenish stores
Suggest take od, then bd then tds for compliance

IV iron if not absorbing or tolerating

167
Q

B12 deficiency anaemia- cause, features, treatment

A

Chronic low intake, pernicious anaemia (anti IF Ab), congenital absence of IF, SBD.

Macrocytic

Oral supplementation

168
Q

folate deficiency anaemia - cause, features, treatment

A

Inadequate intake
Pregnancy, haemolytic anaemia
Coeliac disease, jejunal resection
Drugs (methorexate, trimethoprim)

macrocytic

5mg folic acid PO OD

169
Q

Tension headache - presentation and treatment (episodic and chronic)

A

Band like severe pressure
Can be chronic

When episodic - NSAIDs/paracetamol
Low dose amitriptyline for prevention

170
Q

Cluster headache - presentation and treatment (episodic and chronic)

A

Short unilateral episodes of severe pain around eye with runny nose often accompanying.

SC/nasal triptans used at the start of an attack
12L/min O2 non-rebreather at home for the duration of an attack

Verapamil and alcohol cessation used off license for prophylaxis

171
Q

Migraine - presentation and treatment (episodic and chronic)

A
  • illness +- aura then throbbing headache, n+v, photophobia, dislike movement

NSAID/paracetamol +- antiemetic
Oral triptan if severe

Prophylaxis - topiramate or propanolol (pregnancy)

Mefenamic acid used if related to menstruation

172
Q

Idiopathic intracranial hypertension - presentation and management

A

Raised ICP symptoms; visual disturbances and headaches, pulsatile tinnitus and 6th CN palsy

weight loss, ?steroids, surgical shunt, acetozelamide (carbonic anhydrase inhibitor used to decrease CSF)

173
Q

Raised ICP treatment

A

Elevate head
hyperventilate if intubated; reduced PaCO2 reduces pressure
i.v. mannitol 20%
corticosteroids if tumour

174
Q

Subarachnoid haemorrhage - presentation, diagnosis and treatment

A

Thunderclap, decreased GCS, focal signs, n+v, menigism

CT head
Lumbar puncture (12 hours post presentation) xanthechromia

4 weeks bed rest
BP control
nimodipine - reduces vasospasm
i.v. fluids

coiling or clipping of aneurysm
shunt if hydrocephalus

175
Q

Subdural haemorrhage - acute and chronic - presentation, diagnosis and treatment

A

acute (Sudden acceleration-deceleration injury)
No lucid interval; dilated pupil, reduced GCS

Chronic
Fluctuating headache, drowsiness, confusion

CT head - concave crescent

Surgical drainage

176
Q

Meningitis clinical signs and complications

A

Headache, neck stiffness, fever, photophobia, N+V
Kernig’s sign - flex hip -> pain on leg extension
Brudzinski’s sign - flex neck -> hip and knee flex

Waterhouse-Friderichsen syndrome (WFS) is a group of symptoms caused when the adrenal glands fail to function normally
DIC, sepsis, hydrocephalus, ataxia

177
Q

Meningitis pathogens

A

Neisseria Meningitides - non blanching petechial rash
strep pneumoniae
listeria, haem influ, TB, staph
Viral; entero, hsv, vsv

178
Q

Meningitis investigations

A

Bloods; FBC, U+E, LFT, Lactate, Glucose
Serum PCR for pneumococcal and meningococcal antigens

Lumbar puncture; MC&S, protein, PCR, Glucose, opening pressure
Bacterial: Opening pressure increased, WCC very increased, polymorphs, very Increased protein, Decreased CSF glucose (<50%)
Viral: Opening pressure normal, WCC increased, lymphocytes, Increased protein, normal CSF glucose (>50%)

179
Q

Meningitis treatment

A

The BNF recommend IV cefotaxime (or ceftriaxone) + amoxicillin (or ampicillin) as empirical therapy for adults > 50 years with suspected bacterial meningitis

i.v. benzyl-penicillin if ?meningococcal
i.v. ceftriaxone if not and <60
if >60 add amoxicillin

i.v. dexamethasone can help

Cipro given to close contacts

180
Q

Encephalitis - presentation, diagnosis and treatment

A

Viral - HSV

Normally Mild headache, drowsy, fever, confusion
If severe; HSV-1 can cause necrotising encephalitis of temporals
HSV-2 cause in adults

CT/MRI - diffuse oedema in temporals
LP - increased opening pressure, increased WCC, Increased protein, normal glucose

i.v. aciclovir for 10 days

181
Q

Absence seizures and treatment

A

10-30 seconds loss of consciousness; no motor involvement
More common in children

Ethosuximide
Sodium valproate

182
Q

Myoclonic seizures and treatment

A

Sudden brief muscle contractions bilaterally
Increase with alcohol use and no sleep

Sodium valproate
Levetiracetam

183
Q

Tonic clonic seizures and treatment

A

Rigid body with tongue biting, incontinence etc
Then generalised convulsion, frothing
Post ictal phase; drowsy, coma, confusion, noisy breathing

Sodium valproate,
Lamotrigine
Levetiracetam

184
Q

Focal seizure treatment

A

Lamotrigine
Levetiracetam
Carbamazapine

185
Q

Focal seizure - areas of brain

A

Frontal - motor, speech, Jacksonian march
Parietal - sensory
Occipital - vision
Temporal - lip smacking, chewing *most common area

186
Q

Sodium valproate - MoA and side effects

A

Increases GABA, blocks Na channels

Rash, teratogen, thrombocytopaenia, deranged LFTs

Used in GTC, absence

187
Q

Levetiracetam side effects

A

Mood disturbance, stephens-johnson syndrome

Used for GTC, myoclonic and focal
mainly 2nd line

188
Q

Lamotrigine MoA and side effects

A

Blocks Na channels, decreases glutamate

Skin rash, bone marrow toxicity

189
Q

Carbamazepine MoA and side effects

A

Blocks Na channels

Rash, dizziness, agranulocytosis

Used for focal, GTC, neuropathic pain and manic depressive illness

190
Q

Phenytoin side effects

A

GI, Stevens-Johnson syndrome, rash

191
Q

Vasovagal syncope causes and signs

A

Posture, emotion, pain, heat, dehydration

Prodrome: hot dizzy vision fades tinnitus, n+v, sweaty
Pallor, brevity of shaking, rapid recovery

192
Q

Cardiac syncope

A

Heart disease or exertional in young
ECG normal

193
Q

Acute seizure management
+ If hypo
+ If alcohol withdrawal

A

ABCDE - 100% O2, secure airway, IV access
Bloods- glucose Mg Ca
ECG

IV lorazepam 4mg, repeated in 5 mins of no change
If still no change, phenytoin or Levetiracetam

If hypoglycaemia: iv glucose 50ml 50%
If alcohol withdrawal: I.v. Pabrinex

If >30 mins ITU with GA; thiopentone

194
Q

Driving restrictions with seizures (DVLA)

A

Stop driving after seizure
If single episode: 6 months before reapplying for licence
If multiple: 12 months

195
Q

Amyotrophic lateral sclerosis

A

Most common
Spastic tetraparesis
Muscle wasting and fasciculations, brisk reflexes, upgoing plantars, dysarthria
+- bulbar and pseudobulbar palsy

196
Q

Progressive muscular atrophy

A

MND
Neuronal loss of spinal lower motor neurones
Muscle wasting and fasciculations

197
Q

Primary lateral sclerosis

A

MND
Cortical UMN disease
Progressive spastic tetraparesis and pseudobulbar palsy

198
Q

Progressive bulbar and pseudobulbar palsy

A

MND
LMN and UMN brainstem
Dysarthria, dysphagia, choking, emotional changes
Early respiratory involvement

199
Q

Progressive bulbar and pseudobulbar palsy

A

MND
LMN and UMN brainstem
Dysarthria, dysphagia, choking, emotional changes
Early respiratory involvement

200
Q

General management of MND

A

Palliative MDT
Baclofen for spasticity
DMARDs
NIV

201
Q

Duchenne Muscular dystrophy
Investigations

A

X linked recessive ie only males
Dodgy dystrophy gene; increased muscle breakdown
Onset in children: global weakness, calf pseudohypertrophy (fat replaces muscle) gower’s sign (use hands to stand up)

Increased CK, biopsy, genetics

Poor prognosis early resp involvement and cardiomyopathy

202
Q

Thyroid storm

A

Precipitating events:
thyroid or non-thyroidal surgery
trauma
infection
acute iodine load e.g. CT contrast media

Clinical features include:
fever > 38.5ºC
tachycardia
confusion and agitation
nausea and vomiting
hypertension
heart failure
abnormal liver function test - jaundice may be seen clinically

Management:
symptomatic treatment e.g. paracetamol
treatment of underlying precipitating event
beta-blockers: typically IV propranolol
anti-thyroid drugs: e.g. methimazole or propylthiouracil
Lugol’s iodine
dexamethasone - e.g. 4mg IV qds - blocks the conversion of T4 to T3

203
Q

Becker muscular dystrophy

A

Partially functioning dystrophin
Milder sx compared to Duchenne; 40s life expectancy:

Onset in children: global weakness, calf pseudohypertrophy (fat replaces muscle) gower’s sign (use hands to stand up)

204
Q

Polymyositis and Dermatomyositis
+ investigations + management

A

Polymyositis
Inflammation of proximal striated muscle
Weakness, malaise, fever, weight loss; can cause resp failure

Dermatomyositis
As above + skin involvement
Heliotropic purple rash on face, periorbital oedema, vasculitis over knucles (Gottron papules)

HLAB8/DR3 association with SLE, RA, systemic sclerosis
RF +ve, ANA+ve, increased CK

Prednisolone, DMARDs
IVIG

205
Q

Myotonic dystrophy

A

Autosomal dominant Cl- channelopathy
Muscle weakness and myotonia (unable to relax) affecting face and arms
Associated with frontal balding, cataracts, CVD

206
Q

Inclusion body myositis

A

Proximal and distal muscle wasting
MND mimic

Affects white males in 50s; most common acquired

207
Q

Myasthenia gravis
+ diagnosis + management

A

IgG to Ach post synaptic receptors
associated with autoimmunity - 25% have thymomas

fatiguable weakness; upper limbs, diplopia, ptosis
dysphagia, speech difficulties
reflexes normal

Serum anti AchR Ab
TFTs and CT for thymoma

Avoid glycosides and beta blockers
Neostigmine/pyridostigmine
thymectomy
steroids if hospitalised

208
Q

Guillian Barre Syndrome sx, findings, management

A

Often post-campylobacter inf.
Ascending LMN paralysis, areflexia, no sensory loss
If ocular palsies and ataxia = Miller Fischer

Mainly clinical diagnosis
CSF protein increased

IVIG
Monitor FVC => intubation
SC heparin + stockings

209
Q

Charcot marie tooth

A

progressive neuropathy

210
Q

Friedrich’s ataxia

A

cerebellar ataxia + UMN signs + peripheral neuropathy in childhood

211
Q

Tracheal deviation directions

A

Collapses and pneumonectomies pull the trachea whilst effusions and pneumothorax push it away

212
Q

Recommend Adult Life Support (ALS) adrenaline doses
anaphylaxis:
cardiac arrest:

A

Anaphylaxis: 0.5mg - 0.5ml 1:1,000 IM
Cardiac arrest: 1mg - 10ml 1:10,000 IV or 1ml of 1:1000 IV

213
Q

Anaphylactic shock - haemodynamics and management

A

Decreased SVR, decreased preload, decreased CO

ABCDE
0.5mg IM adrenaline (0.5ml 1:1000)
10mg IV chlorphenamine (antihistamine)
200mg hydrocortisone IV

214
Q

Hypovolaemic shock - haemodynamics and management

A

Increased SVR, decreased preload, decreased CO, decreased BP

Rapid fluid boluses (packed cells/ffp/platelets + tranexamic acid if haemorrhage)

215
Q

Cardiogenic shock - haemodynamics and management

A

Myopathic or arrhythmogenic

increased SVR, increased preload, decreased CO, decreased BP

IV diamorphine 2.5-5mg for pain/SOB/anxiety
furosemide if oedema
ionotropes

216
Q

Neurogenic shock - haemodynamics and management

A

spinal cord transection => increased PS or decreased S

decreased SVR, decreased preload, decreased CO

peripheral vasoconstrictors

217
Q

Thyroid cancer subtypes and tumour markers

A

Papillary - Thyroglobulin
Follicular - Thyroglobulin
Medullary - Calcitonin

218
Q

DVLA hypoglycaemia

A

Notify DVLA
To be able to drive all of the following required:
Awareness
<1 episode with 12 months and not in the last 3 months
Regular review

219
Q

Tests to differentiate between type 1 and 2 diabetes

A

C peptide low in type 1
Autoantibodies (anti-gad) in type 1

220
Q

Mechanical heart valve anticoagulation and INR

A

Warfarin - target INR:
aortic: 3.0
mitral: 3.5

221
Q

Iron deficiency vs anaemia of chronic disease

A

iron deficiency anaemia vs Anaemia of chronic disease
Serum iron
Decreased. Decreased

Total iron-binding capacity
Increased Decreased/normal

Serum ferritin
Decreased Normal/increased

222
Q

most common cause of occupational asthma

A

Isocyanates are the most common cause of occupational asthma
In paint

223
Q

Witnessed cardiac arrest while on a monitor initial treatment/management

A

Witnessed cardiac arrest while on a monitor - up to three successive shocks before CPR

224
Q

If impaired fasting glucose results; what test next and potential findings

A

‘People with IFG should then be offered an oral glucose tolerance test to rule out a diagnosis of diabetes. A result below 11.1 mmol/l but above 7.8 mmol/l indicates that the person doesn’t have diabetes but does have IGT.’

225
Q

Prosthetic heart valves - antithrombotic therapy:

A

bioprosthetic: aspirin
mechanical: warfarin + aspirin

226
Q

When can anti-epileptic drugs be stopped and over what duration?

A

If a pt is seizure free for > 2 years, with AEDs being stopped over 2-3 months

227
Q

Asthma may be diagnosed if any of the following criteria are met (in adults):

A

An exhaled FeNO of 40 parts per billion or greater

A post-bronchodilator improvement in lung volume of 200 ml

A post-bronchodilator improvement in FEV1 of 12% or more

A peak expiratory flow rate variability of 20% or more

An FEV1/FVC ratio <70% (it is an obstructive lung disease)

228
Q

Most common cause of endocarditis:

A

Most common cause of endocarditis:
Staphylococcus aureus
Staphylococcus epidermidis if < 2 months post valve surgery

229
Q

Acceptable changes in U+E when starting an ACE inhibitor e.g. ramipril

A

acceptable changes are an increase in serum creatinine, up to 30% from baseline and an increase in potassium up to 5.5 mmol/l.

230
Q

Do levothyroxine doses need to change in pregnancy

A

Women with hypothyroidism may need to increase their thyroid hormone replacement dose by up to 50% as early as 4-6 weeks of pregnancy

231
Q

Test for latent TB

A

Mantoux test

232
Q

Inducers and inhibitors of cytp450 enzymes

A

Inducers:
antiepileptics: phenytoin, carbamazepine
rifampicin
St John’s Wort
chronic alcohol intake
smoking

Inhibitors:
antibiotics: ciprofloxacin, erythromycin
isoniazid
cimetidine,omeprazole
amiodarone
allopurinol
imidazoles: ketoconazole, fluconazole
SSRIs: fluoxetine, sertraline
ritonavir
sodium valproate
acute alcohol intake

GEM (18 decks)

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