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
2
Q
If giving 30% oxygen, what should PaO2 be ?
A
20
Should be 10 less than that given
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
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)
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
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)
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.
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).
9
Q
Interventions for GORD
A
Offer people a full-dose PPI
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)
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)
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
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)
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)
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)
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
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
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)
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
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
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
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)
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)
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
25
Crohns management - moderate and severe flare, and maintenance.
Mild - oral pred
Severe - i.v. hydrocortisone, parenteral nutrition. Then thiopurines (azathioprine) if needed.
Remission - Thiopurines (azathioprine)
methotrexate 2nd line
26
C. diff investigations
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
27
C. diff toxins
B 1000x worse than A
28
When to do CT in C diff
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
29
C diff Flexible sigmoidoscopy findings
Pseudomembranes manifest as raised yellow or off-white plaques up to 2 cm in diameter scattered over the colonic mucosa
30
C. diff treatment
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
31
Diagnosis of Diabetes
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
32
Situations where HbA1c is not appropriate for diagnosis of diabetes:
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
33
Metformin:
Action
CV Risk
Hypoglycaemia
Weight
Cost
↓HbA1C
Side-effects
Contra-indications
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
34
Gliclazide:
Class
Action
CV Risk
Hypoglycaemia
Weight
↓HbA1C
Side-effects
Contra-indications
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
35
Pioglitazone
Action
CV Risk
Hypoglycaemia
Weight
↓HbA1C
Side-effects
Contra-indications
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
36
Sitagliptin
Action
CV Risk
Hypoglycaemia
Weight
↓HbA1C
Side-effects
Contra-indications
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
37
Glucagon-Like Peptide-1 Agonists:
E.g.
Action
CV Risk
Hypoglycaemia
Weight
Cost
↓HbA1C
Side-effects
Contra-indications
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
38
Sodium Glucose Co-Transporter 2 (SGLT2) Inhibitor:
E.g.
Action
CV Risk
Hypoglycaemia
Weight
Cost
↓HbA1C
Side-effects
Contra-indications
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
39
Anti-diabetic drugs more likely to cause hypoglycaemia
sulfonylureas (gliclazide)
SGLT2 inhibitors (-flozins)
40
Causes of death in DKA
Cerebral oedema (paediatric, young adults), hypokalaemia, ARDS, co-morbid conditions
41
DKA pathogenesis
Progressive metabolic disturbance due to
Insufficient insulin i.e. type I diabetes
Contributory effects of counter-regulatory hormones
==> Metabolic acidosis
42
Clinical features of DKA
Osmotic symptoms
Weight loss
Breathlessness – Kussmaul resps
Abdo pain – children in particular
Leg cramps
Nausea and vomiting
Confusion
Drowsiness
43
Diagnosis of DKA
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
44
Management of DKA
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
45
Management of diabetes
1st, 2nd, 3rd line therapy
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
46
Hyperosmolar hyperglycaemic state diagnosis
Hypovolaemia
hyperglycaemic >30mmol/L without ketones
Osmolality >320 mosmol/kg
(2 (Na) + glucose + urea
> 340 mOsm/kg associated with impairment of consciousness)
47
Clinical features of HHS
Symptoms/signs of intercurrent infection
Severe dehydration
CNS presentation common; Seizures, Aphasia, Hemianopia, Unilateral hyperreflexia, Extensor babinski, Myoclonic jerks, Nystagmus
48
Complications of HHS
Vascular complications:
MI
CVA
Arterial thrombosis
Other complications:
Seizures
Cerebral oedema
Osmotic demyelination
At risk of foot complications
49
HHS management
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
50
Hypoglycaemia symptoms
Acutely unwell
Drowsy
Agitated
Unconscious
Fitting/Seizures
51
Causes of hypoglycaemia in hospital
Missed meals
Reduced appetite
Nil by mouth
AKI (insulin is renally secreted)
Prescription errors: doses, timing, type of insulin
52
Treatment of hypoglycaemia in patients co-operative and able to swallow
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
53
Treatment of hypoglycaemia in patients unconscious/aggressive/un-cooperative
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
54
Neuropathy complications from chronic hyperglycaemia:
Retinopathy
Nephropathy
Neuropathy
Macrovascular
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
55
MEN SYNDROME
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
56
Hypothyroidism
Thyroxine tablets
1.6 mcg/kg body weight
Then titre to give sufficient to suppress TSH to normal
57
Causes of diffuse, multinodular and solitary nodule goitres
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
58
Treatment of hyperthyroid
Thyroidectomy
Carbimazole/ propylthiouracil (used in pregnancy)
RAI
59
Treatment of subclinical hypothyroidism
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
60
Acute thyroiditis management
Propranolol for toxic stage and analgesia
61
Myxoedemic coma and treatment
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
62
Types of thyroid cancer
Papillary good prog
Follicular good prog
Medullary good prog
Anaplastic bad prog
63
Toxic multinodular goitre and treatment
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.
64
Causes of Secondary Hypertension
Cushing’s
Conn’s
Thyroid dysfunction
Acromegaly
Phaeochromocytoma
Hyperparathyroidism
Renal disease
Coarctation of aorta
Obstructive Sleep Apnoea
Alcohol
Cocaine
COCP
Anti-depressant
Herbal remedies
65
Malignant Hypertension
>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
66
Hypertensive retinopathy
-4 grades
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
67
Hypertensive Arteriosclerosis histology
Hypertrophy of media
Fibroelastic thickening of intima
Elastic lamina reduplication
68
HYPERTENSIVE Arteriolosclerosis histology
Replacement of wall structures by amorphous hyaline material
69
Mycotic aneurysm
Mostly caused by endocarditis (infection of heart valve)
Bacterial septicaemia
Infection of arterial wall
70
CCS grading of chest pain
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.
71
Stable angina investigations
ECG, Bloods, CXR, echo
CTCA Gold standard
72
Stable angina management
S/L GTN for all
Betablocker first line (HR 55-60bpm) / calcium channel blocker if not tolerated
Aspirin
Statin
73
Which vessels can be used in CABG
Internal mammary artery
saphenous vein
radial artery
74
3 types of acute coronary syndrome
Unstable angina
NSTEMI
STEMI
75
Differentials for ACS
Peri/Myocarditis
Coronary artery spasm
Tako Tsubo cardiomyopathy
Aortic dissection
Pulmonary embolism
Pneumothorax/pleurisy
Musculo-skeletal/PUD/Chostochondirits, oesophagitis, herpes zoster
76
Acute and longer term management of STEMI
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
77
Mesothelioma diagnosis test
histology, following a thoracoscopy
78
NSTEMI/UA management
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
79
ACS complications
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)
80
Dressler's syndrome
Immune medicated pericarditis
Increased ESR and anti-myocardial antibodies
Different kind of chest pain
Give high dose aspirin/NSAIDs
81
Causes of Elevated Troponins
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
82
Driving restrictions cardiac disease/events (DVLA)
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
83
Tako Tsubo cardiomyopathy
“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.
84
QRS direction in different lead
Positive in I, II, V4-V6
Negative in aVR, V1 and V2
85
QT interval normal duration
Males: <0.40 secs (2 big squares)
Females: <0.44 secs (11 small, or 2 big 1 small)
86
Cardiac axis
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
87
“Tall and Tented” T wave
“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
88
Normal T wave inversion
This can be a normal variant in Leads V1 and III
89
Which heart blocks require pacing
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
90
Delta Wave on the ECG
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
91
STEMI - Chronic ECG Changes
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
92
Tombstoning on ECG
proximal LAD occlusion with poor LV ejection fraction
93
S1Q3T3 pattern
“classic” for PE, but rare:
Deep S-wave (Lead I)
Q wave (Lead III)
Inverted T-wave (Lead III)
94
LBBB ECG
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
RBBB ECG
RSR’ pattern in V1-3 (“M-shaped” QRS complex)
Wide, slurred S wave in lateral leads (I, aVL, V5-6)
MaRRoW
96
Classification of AF
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
CHA2DS2VASc
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
Mechanical valve or moderate to severe mitral stenosis Thrombo-embolic prophylaxis
VKA
99
What Thrombo-embolic prophylaxis is used in AF
DOAC or warfarin (if valvular)
100
Rate control in AF
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
Rate control in non-paroxysmal AF sedentary pt
Digoxin monotherapy only for non-paroxysmal AF in sedentary patients
102
Management of acute onset AF
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
Ablation for AF
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
Bradycardia treatment
If pt has adverse signs:
500ug atropine; repeated up to 3mg if needed
+- External pacing
105
SVT treatment
DCC if pt unstable
Vagal manoeuvres - carotid sinus massage/ valsalva manoeuvre
Adenosine 6mg then 12mg then 12mg
Then DCC
106
VT treatment
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
VF treatment
Emergency defib
After 3 shocks 1mg i.v. adrenaline (0.5ml 1:1000) and
amiodarone 300 mg IV approximately every 3 - 5 min
108
Levels of Severity of Acute Asthma Attacks in Adults
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
Management of acute asthma
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
Discharging acute asthma pt
Be on discharge medication for 24 hours
PEF >75%
Oral and inhaled steroids + bronchodilators
111
COPD exacerbation management
SABA
30mg oral pred 7 days
+- abx
02 if needed
112
COPD long term management
SABA or SAMA
Inhaled corticosteriod
LABA or LAMA
Rescue medication
phosphodiesterase-4 (PDE-4) inhibitor if many exacerbations
113
COPD severity classes
Uses FEV1
Mild >80%
Moderate 50-80%
Severe 30-50%
Very severe <30%
114
Prophylaxis in COPD
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
Long Term Oxygen Therapy criteria
pO2 <7.3 kPa when stable
pO2 <8kPa plus polycythaemia or cor pulmonale
116
Acute COPD exacerbation management if all standard medications fail
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
ABG indications for ventilation
NIV: Type II resp failure - COPD, Obesity, chest wall disorder, neuromuscular
Invasive Type I and II
118
Bronchiectasis on CT
Signet ring
119
Bronchiectasis on examination
Clubbing
Coarse crackles
RHF
inspiratory squeaks
expiratory wheeze
120
Most common bronchiectasis inf. pathogens
Haem influenza
s pneumoniae
pseudomonas
121
Active TB management and ADRs of those drugs
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
Latent TB management and ADRs of those drugs
3 months Isoniazid (with pyridoxine) + rifampicin
Rifampicin - deranged LFTs, pink urine
Isoniazid - peripheral neuropathy pyridoxine should prevent this
123
TB mantoux test results
positive if:
5mm: previous exposure
10mm: risk factors
15mm: anyt indivual
124
Lung cancer types, regions and typical pt
Smoking and central lung - small cell, squamous
Peripheral - adenocarcinoma (increased in asbestosis), large cell
125
Paraneoplastic syndromes
Small cell
ADH - SIADH -> hyponatraemia
ACTH; Cushings
Lambert Eaton syndrome; myasthenia like sx.
Squamous
rPTH; Hypercalcaemia
126
Clinical signs (not sx) of Lung ca
Clubbing
Hypertrophic pulmonary osteoarthropathy; inflamm of small joints in hand
127
Complications of lung ca
Recurrent laryngeal nerve palsy
Phrenic nerve palsy
SVC obstruction
Pancoast syndrome
128
Causes of ILD
Idiopathic
Occupation
Nitrofurantoin, amiodarone, sulfalazine, methotrexate
extrinsic allergic alveolitis
TB, Fungal, viral
Sarcoidosis, RA, SLE, scleroderma
129
ILD on CT
Honeycombing
130
Hypersensitivity pneumonitis (HP) acute and chronic
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
Acute management of Hypersensitivity pneumonitis
O2 and oral pred
132
Hypersensitivity pneumonitis diagnosis
Thorough history!
Bloods (precipitins)
Imaging
Lung function testing
BAL / biopsy?
MDT
133
Simple vs massive coal workers pneumoconiosis
Simple coal worker’s pneumoconiosis = bilateral nodules
Risk of Progressive massive fibrosis (PMF) if exposure continues
134
Asbestos related lung disease
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
CURB65 score
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
HAP management and pathogens
Mild - oral doxy
Severe - i.v. tazocin
Gram negative enterobacteria
2. Methicillin-resistant staphylococcus aureus (MRSA)
3. Pseudomonas
4. Klebsiella
137
Upper and lower zone fibrosis diseases
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
Classes of HF
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
Clinical Signs of heart failure l vs r
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 a galloping horse.)
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
NYHA
I no limitation
II SOB on exertion
III SOB on normal activity
IV SOB at rest
141
Management of acute heart failure
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
Management of chronic heart failure
+ when devices might be indicated
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
ABG for acute HF
Initial type I resp failure then type II
144
Mitral stenosis signs and cause and treatment
Rheumatic fever
Malar flush, small volume pulse, JVP raised, RV hypertrophy
Mid diastolic with opening snap
Balloon valvuloplasty or replacement
145
Mitral regurgitation signs and cause
Post MI, Rheumatic fever, LVH
Systolic thrill
Pansystolic murmur, soft S1; can have 3rd sound
Valve replacement
146
Aortic stenosis signs and cause
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
Aortic regurgitation signs and cause
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
Infective endocarditis RF
Damaged endocardium
Damaged valves
Prosthetic valves
Congenital heart disease
High levels of sustained bacteraemia
IVDUs
Infected intravascular devices
Untreated abscess/collection elsewhere
Surgery
149
Infective endocarditis def
An infectious vegetation on a heart valve
“Pyrexia with a new or changing murmur”
150
Infective endocarditis pathogens and who gets what
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
Clinical signs of infective endocarditis
Murmur
Anaemia
Janeway lesions
Osler’s nodes
Roth’s spots
Pyrexia
Emboli
Nail haemorrhages (splinter haemorrhages)
Splenomegaly
Clubbing
152
Infective endocarditis diagnosis
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
Infective endocarditis treatment
Medical
Antibiotics (correct choice, strength, frequency and duration)
Iv amoxicillin as empirical tx
Vancomycin if prosthetic valves
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
Transudate vs exudate
<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
Pneumothorax treatment
Asymptomatic;
primary: regular review as an outpatient
secondary: inpatient admission for monitoring
symptomatic;
High risk: chest drain
Low risk but >2cm aspiration
156
Tension pneumothorax treatment
100% O2
large bore cannula into 2nd ICS midclavicular line
Chest drain
157
RF for DVT/PE
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
Wells score for DVT
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
May-Thurner syndrome
Compression of the left common iliac vein by the right common iliac artery causes a DVT to form.
160
PE clinical signs
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
Wells score for PE
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
Electrocardiogram (ECG) in PE
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
Types of PE
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
PE management
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
Causes of reduced erythropoiesis
Haematinic deficiency
Iron, folate, B12
2. Bone marrow disorders
Infiltration: Myeloma, leukaemia, lymphoma, myelofibrosis, metastatic cancer
Myelodysplasia
Aplastic anaemia
3. Myelosuppressive drugs
Chemotherapy, co-trimoxazole, multiple others
4. CKD
Reduced EPO
5. Chronic disease/inflammation
Infection, liver disease, autoimmune inflammatory disorders
6. Endocrine dysfunction
Hypothyroid, reduced testosterone
166
iron deficiency anaemia - cause, features, treatment
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
B12 deficiency anaemia- cause, features, treatment
Chronic low intake, pernicious anaemia (anti IF Ab), congenital absence of IF, SBD.
Macrocytic
Oral supplementation
168
folate deficiency anaemia - cause, features, treatment
Inadequate intake
Pregnancy, haemolytic anaemia
Coeliac disease, jejunal resection
Drugs (methorexate, trimethoprim)
macrocytic
5mg folic acid PO OD
169
Tension headache - presentation and treatment (episodic and chronic)
Band like severe pressure
Can be chronic
When episodic - NSAIDs/paracetamol
Low dose amitriptyline for prevention
170
Cluster headache - presentation and treatment (episodic and chronic)
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
Migraine - presentation and treatment (episodic and chronic)
- 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
Idiopathic intracranial hypertension - presentation and management
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
Raised ICP treatment
Elevate head
hyperventilate if intubated; reduced PaCO2 reduces pressure
i.v. mannitol 20%
corticosteroids if tumour
174
Subarachnoid haemorrhage - presentation, diagnosis and treatment
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
Subdural haemorrhage - acute and chronic - presentation, diagnosis and treatment
acute (Sudden acceleration-deceleration injury)
No lucid interval; dilated pupil, reduced GCS
Chronic
Fluctuating headache, drowsiness, confusion
CT head - concave crescent
Surgical drainage
176
Meningitis clinical signs and complications
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
Meningitis pathogens
Neisseria Meningitides - non blanching petechial rash
strep pneumoniae
listeria, haem influ, TB, staph
Viral; entero most common (coxsackie), hsv type 1 , vsv
178
Meningitis investigations
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
Meningitis treatment
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
Encephalitis - presentation, diagnosis and treatment
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
Absence seizures and treatment
10-30 seconds loss of consciousness; no motor involvement
More common in children
Ethosuximide
Sodium valproate
182
Myoclonic seizures and treatment
Sudden brief muscle contractions bilaterally
Increase with alcohol use and no sleep
Sodium valproate
Levetiracetam
183
Tonic clonic seizures and treatment
Rigid body with tongue biting, incontinence etc
Then generalised convulsion, frothing
Post ictal phase; drowsy, coma, confusion, noisy breathing
Sodium valproate,
Lamotrigine
Levetiracetam
184
Focal seizure treatment
Lamotrigine
Levetiracetam
Carbamazapine
185
Focal seizure - areas of brain
Frontal - motor, speech, Jacksonian march
Parietal - sensory
Occipital - vision
Temporal - lip smacking, chewing *most common area
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Sodium valproate - MoA and side effects
Increases GABA, blocks Na channels
Rash, teratogen, thrombocytopaenia, deranged LFTs
Used in GTC, absence
187
Levetiracetam side effects
Mood disturbance, stephens-johnson syndrome
Used for GTC, myoclonic and focal
mainly 2nd line
188
Lamotrigine MoA and side effects
Blocks Na channels, decreases glutamate
Skin rash, bone marrow toxicity
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Carbamazepine MoA and side effects
Blocks Na channels
Rash, dizziness, agranulocytosis
Used for focal, GTC, neuropathic pain and manic depressive illness
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Phenytoin side effects
GI, Stevens-Johnson syndrome, rash
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Vasovagal syncope causes and signs
Posture, emotion, pain, heat, dehydration
Prodrome: hot dizzy vision fades tinnitus, n+v, sweaty
Pallor, brevity of shaking, rapid recovery
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Cardiac syncope
Heart disease or exertional in young
ECG normal
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Acute seizure management
+ If hypo
+ If alcohol withdrawal
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
Driving restrictions with seizures (DVLA)
Stop driving after seizure
If single episode: 6 months before reapplying for licence
If multiple: 12 months
195
Amyotrophic lateral sclerosis
Most common
Spastic tetraparesis
Muscle wasting and fasciculations, brisk reflexes, upgoing plantars, dysarthria
+- bulbar and pseudobulbar palsy
196
Progressive muscular atrophy
MND
Neuronal loss of spinal lower motor neurones
Muscle wasting and fasciculations
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Primary lateral sclerosis
MND
Cortical UMN disease
Progressive spastic tetraparesis and pseudobulbar palsy
198
Progressive bulbar and pseudobulbar palsy
MND
LMN and UMN brainstem
Dysarthria, dysphagia, choking, emotional changes
Early respiratory involvement
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Progressive bulbar and pseudobulbar palsy
MND
LMN and UMN brainstem
Dysarthria, dysphagia, choking, emotional changes
Early respiratory involvement
200
General management of MND
Palliative MDT
Baclofen for spasticity
DMARDs
NIV
201
Duchenne Muscular dystrophy
Investigations
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
Thyroid storm
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
Becker muscular dystrophy
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
Polymyositis and Dermatomyositis
+ investigations + management
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
Myotonic dystrophy
Autosomal dominant Cl- channelopathy
Muscle weakness and myotonia (unable to relax) affecting face and arms
Associated with frontal balding, cataracts, CVD
206
Inclusion body myositis
Proximal and distal muscle wasting
MND mimic
Affects white males in 50s; most common acquired
207
Myasthenia gravis
+ diagnosis + management
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
Guillian Barre Syndrome sx, findings, management
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
Charcot marie tooth
progressive neuropathy
210
Friedrich's ataxia
cerebellar ataxia + UMN signs + peripheral neuropathy in childhood
211
Tracheal deviation directions
Collapses and pneumonectomies pull the trachea whilst effusions and pneumothorax push it away
212
Recommend Adult Life Support (ALS) adrenaline doses
anaphylaxis:
cardiac arrest:
Anaphylaxis: 0.5mg - 0.5ml 1:1,000 IM
Cardiac arrest: 1mg - 10ml 1:10,000 IV or 1ml of 1:1000 IV
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Anaphylactic shock - haemodynamics and management
Decreased SVR, decreased preload, decreased CO
ABCDE
0.5mg IM adrenaline (0.5ml 1:1000)
10mg IV chlorphenamine (antihistamine)
200mg hydrocortisone IV
214
Hypovolaemic shock - haemodynamics and management
Increased SVR, decreased preload, decreased CO, decreased BP
Rapid fluid boluses (packed cells/ffp/platelets + tranexamic acid if haemorrhage)
215
Cardiogenic shock - haemodynamics and management
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
Neurogenic shock - haemodynamics and management
spinal cord transection => increased PS or decreased S
decreased SVR, decreased preload, decreased CO
peripheral vasoconstrictors
217
Thyroid cancer subtypes and tumour markers
Papillary - Thyroglobulin
Follicular - Thyroglobulin
Medullary - Calcitonin
218
DVLA hypoglycaemia
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
Tests to differentiate between type 1 and 2 diabetes
C peptide low in type 1
Autoantibodies (anti-gad) in type 1
220
Mechanical heart valve anticoagulation and INR
Warfarin - target INR:
aortic: 3.0
mitral: 3.5
221
Iron deficiency vs anaemia of chronic disease
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
most common cause of occupational asthma
Isocyanates are the most common cause of occupational asthma
In paint
223
Witnessed cardiac arrest while on a monitor initial treatment/management
Witnessed cardiac arrest while on a monitor - up to three successive shocks before CPR
224
If impaired fasting glucose results; what test next and potential findings
'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
Prosthetic heart valves - antithrombotic therapy:
bioprosthetic: aspirin
mechanical: warfarin + aspirin
226
When can anti-epileptic drugs be stopped and over what duration?
If a pt is seizure free for > 2 years, with AEDs being stopped over 2-3 months
227
Asthma may be diagnosed if any of the following criteria are met (in adults):
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
Most common cause of endocarditis:
Most common cause of endocarditis:
Staphylococcus aureus
Staphylococcus epidermidis if < 2 months post valve surgery
229
Acceptable changes in U+E when starting an ACE inhibitor e.g. ramipril
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
Do levothyroxine doses need to change in pregnancy
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
Test for latent TB
Mantoux test
232
Inducers and inhibitors of cytp450 enzymes
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
