1
Q
Up and til what age are newborns offered regular health and development reviews?
A
2 years old
2
Q
When is the heel prick test performed on newborns?
A
at 5 and 8 days after birth
3
Q
What does a heel prick test screen for?
A
sickle cell disease (SCD)
cystic fibrosis (CF)
congenital hypothyroidism (CHT)
phenylketonuria (PKU)
medium-chain acyl-CoA dehydrogenase deficiency (MCADD)
maple syrup urine disease (MSUD)
isovaleric acidaemia (IVA)
glutaric aciduria type 1 (GA1)
homocystinuria (HCU)
4
Q
When is the first new baby review performed?
A
in the first 1-2 weeks after birth
5
Q
What occurs at the 6-8 week check?
A
Comprehensive physical examination of baby (eyes, heart, hips, testicles, weight, length, circumference)
Discussion of baby vaccinations
Check up on mother’s mental + physical health as well
6
Q
When are the baby vaccinations offered?
A
8 weeks
12 weeks
16 weeks
12 months
Before child starts school (around 4)
7
Q
When are baby reviews performed?
A
Just after birth
1-2 weeks
6-8 weeks
9-12 months
2-2.5 years
8
Q
What vaccination is given at 8 weeks?
A
5 in 1 (diphtheria, tetanus, whooping cough, polio and Hib disease)
9
Q
What are the routes of administration for paracetamol?
A
PO (oral), rectally (PR), intravenously (IV)
10
Q
What is the pain ladder?
A
Guidelines for the use of drugs in the management of pain
11
Q
What are the steps in the pain ladder?
A
- Non-opioid analgesics (e.g. NSAIDs) ± adjuvant analgesic
- Weak opioids ± non-opioid ± adjuvant analgesic
- Strong-opioid analgesic ± non-opioid ± adjuvant analgesic
- Minimal invasive intervention ± non-opioid ± adjuvant analgesic
12
Q
What is an adjuvant analgesic?
A
Drugs with a primary indication other than pain but which have analgesic properties e.g. antidepressants, local anaesthetics, corticosteroids, bisphosphonates
13
Q
What is the method of action of NSAIDs?
A
Inhibit the action of cyclooxygenase enzymes which catalyse the conversion of arachidonic acid into prostaglandin H2, the precursor of PGs and thromboxane. Their effects are anti-inflammatory, antipyretic and analgesic
14
Q
What are Non-selective vs selective NSAIDs?
A
Non-selective NSAIDs block both COX-1 and COX-2 inhibitors (high risk of side effects)
Selective NSAIDs block only COX-2
15
Q
What are the possible side effects of non-selective NSAIDs?
A
easy bleeding, skin rash
bronchospasm
dyspepsia, n+v, gastric ulceration, haemorrhage
nephritis
16
Q
What are 3 examples of NSAIDs?
A
Aspirin
Ibuprofen
Naproxen
17
Q
What are 2 examples of selective NSAIDs?
A
etoricoxib
celecoxib
18
Q
What is the difference between COX-1 and COX-2?
A
COX-1 = active in normal physiology
COX-2 = active in inflammatory response
19
Q
What are the investigations for IBD?
A
Routine bloods: FBC, U+Es, TFTs
CRP (blood test)
Faecal calprotectin (stool sample)
Endoscopy with biopsy (GS)
USS, CT + MRI
20
Q
What are the main differences between UC and Crohn’s disease?
A
- Crohn’s affects the whole GI tract (mouth->anus) and UC affects the lower GI tract only (colon->rectum)
- in Crohn’s the inflammation affects the entire thickness of the intestinal lining, UC is only the innermost lining
- CD = patchy affected areas, UC = uniformly affected
- complications of CD = strictures, fissures + fistulas, complications of UC = haemorrhage + toxic megacolon
- Smoking causing increased risk of CD but decreased of UC
- cancer risk is higher with UC
21
Q
What are the differences between IBD and IBS?
A
- IBD = chronic, incurable digestive disease, IBS = functional bowel disorder
- IBD can cause urgency, fatigue, weight loss and malnutrition alongside the abdominal cramps, bloating, gas, mucus in stool, diarrhoea and/or constipation seen in IBS
- IBD can cause permanent damage to GI tract but IBS just causes inflammation
- surgery is often implicated in IBD treatment but not for IBS
- IBD can cause complications affecting joints, eyes, kidneys, skin and bones whereas main complication of IBS is impaired QOL
22
Q
What are the red flag signs/symptoms for IBS/IBD?
A
weight loss
blood in stools
anaemia
fever
urgency
abdominal pain
23
Q
What are the mechanisms of action of antidiarrhoeals?
A
- Adsorbents - help eliminate the causative toxin or bacteria by coating the walls of the GI tract and binding the pathogen for elimination in the stool
- Antimotility agents - slow peristalsis either by acting on the smooth muscle of the GI tract to inhibit propulsive motility and decrease gastric acid secretion (anticholinergics), or by decreasing the flow of fluids and electrolytes in the bowel and slowing the movement of the bowel to reduce the number of bowel movements (opioid-like)
- Probiotics - help to restore normal bacteria in the lower GI tract
24
Q
What are examples of antidiarrhoeals of the 3 types?
A
Adsorbents: bismuth subsalicyclate
Antimotility: hyoscyamine (anticholinergic), loperamide (opiate-like)
Probiotics: lactobacillus
25
What are the methods of action of laxatives?
1. Osmotic laxatives - draw water into the lumen to increase intestinal peristalsis
2. Bulk-forming agents - draw water into the stool forming a soft, bulky mass, which stimulates intestinal peristalsis
3. Stimulant laxatives - irritate nerve endings in the intestinal walls, thereby stimulating smooth muscle contraction and intestinal peristalsis
4. Emollient laxatives - act as surfactant that allows the water to penetrate the stool and make it softer
26
Give an example of each of the 4 types of laxatives?
Osmotic - magnesium hydroxide (milk of magnesia), lactulose
Bulk-forming agent - methylcellulose, polycarbophil
Stimulant - bisacodyl, senna
Emollient - docusate
27
What occurs when someone taking the combined oral contraceptive pill (cOCP) has diarrhoea?
Severe diarrhoea (6-8 watery stools in 24 hrs) causes decreased absorption in the GI lumen and so the pill may not be absorbed or only partially absorbed reducing its contraceptive effect.
28
What other contraceptive options should be considered for patients who have severe diarrhoea or chronic bowel disorders?
progesterone only pill, IUD, IUS, condoms, injections, implant
29
Which medications are used prophylactically for MI?
BBs, ACE-is + CCBs to treat hypertension
Statins for hyperlipidaemia
Diabetes medications (e.g. metformin)
Anti-thrombotic agents (e.g. aspirin)
30
What is seen on ECG over the course of a heart attack?
Onset of pain - normal ECG, T wave beginning to grow taller
Within an hour - noticeably elevated ST segment (indicates onset of myocardial necrosis)
If thrombolysis is administered - 50% reduction of ST segment elevation (within 90 mins of administration) is sign of success, T wave inverted and deeper (sign of re-perfusion of damaged area)
24hrs later - ST segment returned to isoelectric line, T wave may remain inverted
Months later - relatively normal, T wave may still be inverted and deep Q wave may also remain (indicating myocardial tissue death)
31
Which drugs are used in treatment for heart failure
ACE-i + B-blocker for all patients
+ spironolactone + furosemide
+ consider cardiac resynchronisation therapy
32
What is the mechanism of action of ACEis?
Inhibit angiotensin-converting enzyme which prevents the conversion of angiotensin I to angiotensin II. Angiotensin II causes vasoconstriction of blood vessels and so ACE-inhibitors have a vasodilatory effect, helping to reduce blood pressure.
33
What are the side effects of ACE-is?
Dry cough (result of kinins accumulating in lungs, seen in 10-30% patients)
Hyperkalaemia
Fatigue
Dizziness (hypotension)
Headaches
Loss of taste
34
What are examples of ACE-is?
Ramipril
Lisinopril
Enalapril
35
Why are ACE-is not used in the black african population?
ACE-is are less effective in black patients due to their tendency towards a lower renin state and lower cardiac output with increased peripheral state. (RAAS less implicated as the cause of the hypertension)
CCBs are usually the first line treatment.
36
What are the nice guidelines for medical management of Type II diabetes?
1st line: metformin (titrated starting with 500mg OD)
2nd line: metformin + sulfonylurea, pioglitazone, DPP-4 inhibitors, SGLT-2 inhibitors or GLP-1 mimetics
3rd line: triple therapy --> metformin + 2 of the second line drugs OR metformin + insulin
37
What is the action of metformin?
It's a biguanide which increases insulin sensitivity and decreases liver production of glucose
38
What are the major side effects of metformin?
diarrhoea + abdo pain
lactic acidosis
weight neutral and does NOT typically cause hypoglycaemia
39
What is the method of action of pioglitazone?
increases insulin sensitivity and decreases liver production of glucose
40
What are the major side effects of pioglitazone?
weight gain
fluid retention
anaemia
heart failure
extended use can increase risk of bladder cancer
Does NOT typically cause hypoglycaemia
41
What is the method of action of sulfonylureas?
stimulate insulin release from the pancreas
42
what are the major side effects of sulfonylureas?
weight gain
hypoglycaemia
increased risk of cardiovascular disease and myocardial infarction when used as monotherapy
43
What is the action of DPP-4 inhibitors?
Inhibit the DPP-4 enzyme and increase GLP-1 activity as a result. GLP-1 is an incretin and increases insulin secretions, inhibits glucagon production and slows absorption by the GI tract
44
What are the major side effects of DPP-4 inhibitors?
GI tract upset
symptoms of upper respiratory tract infection
pancreatitis
45
What is the action of GLP-1 mimetics?
To mimic the action of GLP-1, increasing insulin secretions, inhibiting glucagon production and slowing absorption by the GI tract
46
What are the major side effects of GLP-1 mimetics?
GI tract upset
weight loss
dizziness
*low risk of hypoglycaemia
47
What is the action of SGLT-2 inhibitors?
block the action of SGLT-2 proteins which are responsible for reabsorbing glucose from the urine in the proximal tubules of the kidneys
48
What are the major side effects of SGLT-2 inhibitors?
glycoseuria
increased rate of UTIs
weight loss
diabetic ketoacidosis
low limb amputation (more common in patients on canagliflozin)
49
What is tested for in urinalysis?
blood
protein
pH
ketones
nitrates
glucose
leukocytes
50
What are 5 major differences between osteoarthritis and rheumatoid arthritis?
- RA is an autoimmune disorder whereas OA is caused by mechanical wear and tear
- RA affects mostly the hands (MCP, PIP joints) but not the DIPs, whereas OA affects large, weight bearing joints, CMC, DIP + PIP
- RA is symmetrical and OA is initially asymmetrical though can become asymmetrical
- RA is characterised by morning stiffness which improves with use whereas OA joints cause pain following use and improve with rest
- RA is seen in adults of all ages whereas OA is seen mostly in the elderly
51
What is the treatment for osteoarthritis?
Education/lifestyle advice/physiotherapy/occupational therapy
Analgesia:
Paracetamol and topical NSAIDs
Oral NSAIDs and consider also prescribing a PPI
Consider opiates such a codeine and morphine
Intra articular steroid injections
Joint replacement in severe cases
52
What is the management for rheumatoid arthritis?
short course of steroids at first presentation
DMARD (methotrexate)
NSAID analgesia
Intra-articular steroid injection for severe pain
Biologics (infliximab, rituximab)
53
What are the differences between gout and pseudogout?
- gout is most commonly seen in obese males who consume large volumes of beer whereas pseudogout is seen in elderly patients with hyperparathyroidism, haemochromatosis, hypophosphataemia, osteoarthritis
- the acute presentation of gout is acute monoarthropathy typically in the MTP of first toe whereas pseudogout is acute monoarthropathy typically of knee
- the crystals in gout are made up of monosodium urate whereas in pseudogout they are calcium pyrophosphate
- gout crystals are negatively birefringent needles and pseudogout crystals are weakly positive birefringent rhomboids
- on XR gout presents with well-defined 'punched-out' periarticular erosions and pseudogout shows chondrocalcinosis
54
What is methotrexate and what is its mode of action?
Methotrexate is a disease-modifying anti rheumatic drug which inhibits dihydrofolate reductase resulting in a deficiency in the cellular pools of thymidylate and purines leading to a decrease in nucleic acid synthesis. This suppresses the immune system and reduces inflammatory response.
55
What are LUTS?
a range of symptoms affecting the control and quality of micturition in the lower urinary tract
56
What percentage of men over 50 years suffer from LUTS?
50%
57
WHat are the causes of LUTS?
BPH
UTIs
bladder cancer
prostate cancer
detrusor muscle weakness
pelvic floor dysfunction
chronic prostatitis
urethral stricture
pelvic tumours
neurological disease
lifestyle factors (excess caffeine, alcohol, drinking late at night )
58
What are the storage LUTS?
when bladder should be storing urine
urgency
frequency
incontinence
nocturia
59
What are voiding LUTS
occur when bladder outlet is obstructed
poor stream
intermittency
straining
incomplete emptying
dribbling
hesitancy
60
What are the red flags for LUTS?
haematuria + dysuria
61
What is the treatment for BPH?
lifestyle changes
decrease caffeine
A-blocker (tamsulosin) - relax muscles in prostate and bladder so that urine can flow more easily
5-alpha reductase inhibitors (finasteride) - decrease testosterone production --> ↓size of prostate
62
What are the side effects of tamsulosin?
dizziness, fatigue, inability to ejaculate, headaches, nasal congestion
63
What are the side effects of 5-alpha reductase inhibitors?
reduced libido, reduced semen volume, weaker erections in 5-15%, depression
64
Why is the PSA test unreliable>
High specificity for prostate cancer detection but low sensitivity so false-positives are common and can create anxiety and lead to additional medical procedures (e.g. biopsy) which can be harmful
65
What is the method of action of sodium valproate?
increases the amount of GABA in the brain which blocks transmission across nerves in the brain and helps to slow neural transmission, reducing or preventing manic episodes
66
What is the method of action of carbamazepine?
it stabilises the electrical activity in the brain and nerves by stopping electrical signals from building up in the nerve cells in the brain
it also reduced the release of glutamate which helps prevent seizures
67
What are the side effects of carbamazepine?
dizziness
fatigue
nausea/vomiting
headaches
dry mouth
weight gain
68
What are the side effects of sodium valproate?
abdominal pain
nausea/vomiting
dry or sore mouth
tremors
fatigue
headaches
weight gain
thinning hair
69
What are the contraindications for sodium valproate?
hepatic disorders
hypersensitivities
urea cycle disorders
mitochondrial disorders
pregnancy
70
What are the contraindications for carbamazepine?
bone marrow depression
hypersensitivity
Phase 2A
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