GP Flashcards
What are the causes of tonsillitis?
Viral → most cases
Bacterial:
- group A strep. pyogenes (most common)
- strep. pneumoniae
- haemophilus influenzae
- staph aureus
Describe the presentation of tonsillitis?
- sore throat
- fever ↑ 38
- pain on swallowing
- o/e tonsils will be red, inflamed & enlarged
- tonsils may or may not have exudates
- may be anterior cervical lymphadenopathy
What is the centor criteria?
Used to estimate the probability that tonsillitis is due to bacterial infection and will benefit from abx
A point is given for each of the following features:
- fever ↑ 38
- tonsillar exudates
- absence of cough
- tender anterior cervical lymph nodes
Score of 3 or more means appropriate to offer abx
What is the FeverPAIN score?
Alternative to Centor Criteria
Fever during previous 24 hours
Pus on tonsils
Attended within 3 days of onset of symptoms
Inflamed tonsils
No cough of coryza
4-5 points is ~65% probability of bacterial tonsillitis
Management of tonsillitis?
Admission if immunocompromised, dehydrated, stridor, respiratory distress or peritonsillar abscess/cellulitis
Viral –> analgesia, frequent hydration, safety net → patient to return if fever ↑38 or pain has not settled in 3 days
Bacterial → abx if centor is 3 or more of if FeverPAIN is 4 or more, OR young infant, immunocompromised etc consider delayed rx
- penicillin V (phenoxymethylpenicillin) for 5-10 days or clarithromycin if allergic to penicillins
Define hypertension
Persistently raised high blood pressure:
clinical BP of 140/90 or above
ambulatory/home BP of 135/85 or above
Primary vs secondary hypertension
Primary = no identifiable underlying cause (has risk factors)
Secondary = underlying disease process causing HTN
Causes of secondary hypertension?
ROPED:
Renal disease (commonly renal artery stenosis)
Obesity
Pregnancy (pre-eclampsia)
Endocrine (hyperaldonsteronism/Cushing’s)
Drugs (alcohol, stimulants, steroids, NSAIDs, oestrogen, liquorice)
Hypertension risk factors?
Non-modifiable: increasing age, african heritage, family history
Modifiable risk factors: obesity, sedentary lifestyle, alochol, smoking, high sodium, stress
What is malignant hypertension?
An acute, severe elevation of BP → usually diagnosed due to retinal signs eg papilloedema, flame shaped haemorrhages, hard exudates, cotton wool spots
What are the complications of hypertension?
IHD eg angina or acute coronary syndrome
CVA eg stroke or haemorrhage
Vascular disease eg peripheral arterial disease, aortic dissection, aortic aneurysm
Hypertensive retinopathy
Hypertensive nephropathy
Vascular dementia
LVH
Heart failure
What are the stages of hypertension?
Stage 1: clinic 140/90 home 135/85
Stage 2: clinic 160/100 home 150/95
Stage 3: 180/120
Diagnosing hypertension?
Patients with clinic BP of 14/90 or more should have 24 ambulatory BP or home readings to confirm diagnosis
NICE recommends measuring BP in both arms → if difference is more than 15, sue the reading from the arm with the higher pressure
What are the investigations all patients with newly diagnosed BP should have?
Calculate QRISK → if above 10%, should be offered a statin
Identify end organ damage:
Urine albumin:creatinine ratio for proteinuria & dipstick for microscopic haematuria to assess kidney damage
Bloods: HbA1C, renal function, lipids
Fundus exam: for hypertensive retinopathy
ECG: for cardiac abnormalities, including left ventricular hypertrophy
What is the drug management for hypertension?
Step One:
HTN w/ T2DM: ACEi (ramipril) or ARB (candesartan)
HTN age <55 not black: ACEi or ARB
HTN age >55: CCB (amlodipine)
HTN w/ black heritage, any age: CCB
Step Two:
Can combine an ACEi/ARB with CCB or thiazide-like diuretic (indapamide)
Can combine a CCB with ACEi or ARB or thiazide-like diuretic
Step Three:
Combine all 3 drugs
Stage 4:
Serum potassium <4.5 or equal: all 3 drugs PLUS spironolactone
Serum potassium >4.5: all 3 drugs PLUS alpha blocker (doxazosin) OR beta blocker (atenolol)
What is infectious mononucleosis?
Condition caused by EBV (most common manifestation of EBV) →virus found in saliva of infected individuals, infection spread by sharing saliva, can be infectious for several weeks, causes few symptoms in childhood, more severe in adulthood/teenagers
What are the signs and symptoms of infectious mononucleosis?
Fever
Sore throat
Fatigue
Lymphadenopathy
Tonsillar enlargement
Splenomegaly
EXAM TIP: teen who comes in with sore throat and gets rash after taking amoxicillin
Mono causes a very itchy maculopapular rash in response to amoxicillin or cefalosporins
Tests to identify infectious mononucleosis?
Heterophile antibodies: body produces heterophile antibodies in response to mono but aren’t specific to the EBV antigens and takes up to 6 weeks for the antibodies to be produced
- monospot test: add horse RBCs to heterophile antibodies and they react to give a +tive result
- Paul-Bunnel test: similar to monospot but uses sheep RBCs
100% specific to IM but only 70-80% sensitive
Specific antibody tests:
EBV antibodies target the viral capsid antigen
The IgM antibody rises early and suggests acute infection
The IgG antibody persists after the condition and suggests immunity
Management of infectious mononucleosis?
Usually self limiting → acute illness lasts 2-3 weeks but can leave patient with severe fatigue for months once infection is cleared
- patients should avoid alcohol & contact sports
Complications of infectious mononucleosis?
Splenic rupture
Glomerulonephritis
Haemolytic anaemia
Thrombocytopenia
Chronic fatigue
Define chronic kidney disease?
Describes a chronic reduction in kidney function, which tends to be permanent & progressive
What are the causes of CKD?
Diabetes
HTN
Age related decline
Glomerulonephritis
Polycystic kidney disease
Medications eg NSAIDS, PPIs, lithium, ramipril
Risk factors for CKS?
Old age
HTN
Diabetes
Smoking
Use of medication that affects the kidneys
How do patients with CKD present?
Itching
Loss of appetite
Nausea
Oedema
Muscle cramps
Peripheral neuropathy
Pallor
Hypertension
What are the investigations for CKD?
eGFR: 2 tests, 3 months apart to confirm diagnosis
Proteinuria: can be checked using urine albumin:creatinine ratio, with a result of 3mg/mmol or more as significant
Haematuria: can be checked using a urine dipstick → can be indicator of bladder cancer (painless haematuria)
Renal USS: can be used to investigate patients with accelerated CKD, haematuria, family history of polycystic kidney disease or evidence of obstruction
How is CKD staged? (G score)
The G score is based on the eGFR:
G1: eGFR >90
G2: eGFR 60-89
G3a: eGFR 45-59
G3b: eGFR 30-44
G4: 15-29
G5: eGFR <15 → end stage renal failure
How is CKD staged? (A score)
A score is based on the albumin:creatinine ratio
A1: <3mg/mmol
A2: 3-30mg/mmol
A3: >30mg/mmol
The patient does not have CKD if they have a score of A1 combined with G1 or G2. They need at least an eGFR of <6o or proteinuria for a diagnosis
What are the complications of CKD?
Anaemia
Renal bone disease
Cardiovascular disease
Peripheral neuropathy
Dialysis related problems
How is CKD managed?
Aims of management: slow the progression of the disease, reduce the risk of cardiovascular disease, reduce the risk of complications, treat complications
Slow progression of the disease: optimise diabetic control, optimise hypertensive control, treat glomerulonephritis
Reducing the risk of complications: exercise, maintaining a healthy weight, stop smoking, special dietary advice phosphate, sodium, potassium, water intake, offer statin for primary prevention of cardiovascular disease
Treating complications:
- oral sodium bicarbonate to treat metabolic acidosis
- iron supplement & erythropoietin to treat anaemia
- vitamin D to treat renal bone disease
- dialysis in end stage renal failure
- renal transplant in end stage renal failure
Describe anaemia of chronic kidney disease?
Damaged kidney cells in CKD cause a drop in erythropoietin and so a drop in RBC production and anaemia
Anaemia can be treated with erythropoiesis stimulating agents eg exogenous erythropoietin
Blood transfusions should be limited as they can lead to allosensitisation and so transplanted organs are more likely to be rejected
Iron deficiency should be treated before offering erythropoietin.
Describe renal bone disease?
Also known as chronic kidney disease-mineral and bone disorder
Define hypothyroidism?
Refers to insufficient thyroid hormones T3 & T4. Most prevalent in women and the elderly.
Describe the causes of primary hypothyroidism
(problem with the thyroid producing inadequate thyroid hormones):
- autoimmune including Hashimoto’s & atrophic hypothyroidism
-iodine deficiency
-drugs eg treatments for hyperthyroidism
-lithium
-amiodarone
Describe the causes of secondary hypothyroidism
(also known as central hypothyroidism is a problem with the pituitary gland and leads to under-stimulation of the thyroid):
- tumours eg pituitary adenoma
- surgery to the pituitary
- radiotherapy
- trauma
What is Hashimoto’s?
Autoimmune condition where T Cells attack the thyroid → Hashimoto’s can cause goitre unlike atrophic hypothyroidism
What are the antibodies associated with Hashimoto’s?
anti-TPO (anti-thyroid peroxidase) and anti-Tg (anti-thyroglobulin antibodies)
How do patients with hypothyroidism present?
Appearance: puffy eyes, dry skin, brittle hair, very thin hair, overweight
Other symptoms: cold intolerance, fatigue, tiredness, headaches, sluggish reflexes, fluid retention, heavy or irregular periods, constipation, depression, poor memory, bradycardia, hypertension
Goitre: hashimoto’s can cause goitre/goitre is normally caused by iodine deficiency
Describe thyroid function blood test results and what they mean (hypothyroidism)
TSH ↑ and T4 ↓ : primary hypothyroidism
TSH ↓ and T4 ↓ : secondary hypothyroidism
What is the management of hypothyroidism?
Oral levothyroxine is a synthetic version of T4 and is titrated based on the TSH level around every 4 weeks
What are the risk factors for iron deficiency anaemia?
Vegetarian/vegan
H. pylori infection
Pregnancy
Young children & adolescents
IBD
Coeliac disease
Drugs eg PPIs
Describe the pathophysiology of iron deficiency anaemia
Bone marrow requires iron to produce haemoglobin so low iron levels lead to impaired Hb production.
Not enough Hb for normal sized RBC so bone marrow starts producing microcytic RBCs, which appear pale (hypochromic) because they contain less Hb
The microcytic RBCs can’t carry as much oxygen to the tissues (hypoxia). This hypoxia signals to the bone marrow to increase RBC production leading to the bone marrow to produce incompletely formed RBCs.
Iron deficiency also results in defection production of mitochondrial enzymes that generate ATP necessary for growth and development of fast growing tissues eg nails and hair
Describe the signs and symptoms of iron deficiency anaemia
Signs: pallor, conjunctival pallor, glossitis, koilonychia (spoon shaped nails), angular stomatitis
Symptoms: fatigue, dyspnoea, dizziness, headache, nausea, bowel disturbance, hair loss, abnormal cravings (pica)
What are the investigations for iron deficiency anaemia?
FBC: low Hb, low MCV, low MCHC
Iron studies:
- serum iron
- serum ferritin: low
- total iron binding capacity: can be used as a marker for how much transferrin is in the blood (increased in anaemia)
- transferrin saturation: gives a good indication of the total iron in the body (decreased in anaemia)
What is the management of iron deficiency anaemia?
- treat the underlying cause
- oral iron supplements: ferrous sulphate or ferrous fumarate → S/E constipation, black coloured stools, diarrhoea, nausea and dyspepsia
- iron transfusion
- blood transfusions
