GP core conditions Flashcards
Asthma: patho physiology
Patho physiology:
• IgE mediated inflammatory response. This is the Ig dealing with allergens. If an allergen is encountered it can trigger response of:
• Bronchial muscle contraction
• Mast cell+ basophil degranulation (causing inflammation of airway)
• Increased mucus secretion
Non allergic asthma has similar symptoms but without allergen, can have other triggers such as:
Viral
Drugs (beta-blockers and NSAIDs)
Exercise and cold air- dries airways so can trigger inflame response
asthma: symptoms
Clinical triad:
• Dry chronic cough (worse at night)
• SOB
• Expiratory wheeze
asthma: acute signs
Acute signs: • Tachypnoea • Expiratory wheeze • Hyperinflated chest • PEFR <33% • Paradoxical pulse (bp falls on inspiration)
Asthma:Investigations
spirometry: FEV1/ FVC < 70%
you can perform an FEV1 reversibility test
Asthma: Management
Under 5s
- Short acting B2 agonist
- +Regular low dose inhaled corticosteroid (ICS) for 8 weeks)
- +LTRA (leukotriene receptor antagonist) (montelukast)
- Increase dose of steroids
- Oral steroids
- Refer
Asthma: Management
Over 5s
- SABA (salbutamol or terbutaline)
- ICS (beclometasone or fluticasone) +oral LTRA
- ICS +inhaled LABA (salmeterol)
- Moderate dose ICS +LABA
- High dose ICS
- Add theophylline
- Oral steroids (prednisolone) + refer
Heart Failure: pathophysiology
CO= SV x HR. There is decreased SV.
systolic failure: more common, cannot contract fully –> causes like ishcaemic heart disease
Diastolic failure: due to hypertrophy, pericardium problems (pericarditis, tamponade)
RSHF: can come from a result of lung diseases causing increase in vascular resistance–> pulm. hypertension (cor pulmonale)
other causes: hypertension (most common) cardiomyopathies Arrythmias (AF) Mitral incompetence
Heart failure: Symptoms
Cough (esp at night). pink frothy sputum PND decreased exercise tolerance SOB sweating and clammy
Heart failure: signs
Pitting odoema in ankles pulmonary odeoma- LSHF Sacral odeoma and increased JVP-- RSHF tachycardic expiratory fine crackles hepatomegaly (due to portal hypertension) - ascites weight gain/ weight loss displaced apex beat
Heart failure: Diagnosis
gold standard: use echocardiogram – measures Ejection fractions
in GP- BNP (relates to damaged heart muscle)
Framlingham criteria
New York Hear Association classification
Heart failure: investigation (1)
Echo
ECG
Chest X- ray
Bloods
Heart failure: investigations (2)
Ecg - can spot causes: AF, MI (inverted T waves- partial ischaemia, pathological Q waves- full ischaemia), can see axis deviation (due to hypertrophy), larger R waves
Bloods- FBC, UandEs, TFTs, LFTs, BNP
CXR- A- Alveolar odema
B- Kerley B lines
C- cardiomegaly
D- upper lobe deviation (vessels pointing up)
E- effusions- bilateral
HF, Management: acute
Oxygen
Morphine
Furosemide - 40-80 mg IV
GTN spray - vasodilator (if compensating HF, refer to senior to not tip person into cardiogenic shock)
HF, management: chronic
Diuretics: FUROSEMIDE, spironolactone
ACEi - lisinopril/ ramipril
B BLOCKER - bisoprolol
digoxin - decreases heart rate and increases heart contractility
Diabetes Mellitus: Pathophysiology (1)
Type 1: autoimmune destruction of beta cells in Islets of Langerhans in the pancreas –> this results in reduced production of insulin. As a result less glucose is taken from blood into cells and converted to glycogen.
Type 2: Beta cells are intact but secrete less insulin, other cells also become less insulin sensitive.
DM: Pathophysiology (2)
100% of filtered glucose in urine in kidneys should be reabsorbed. But due to large amount of glucose, the transport tubules are at full capacity so glucose remains in urine. This causes water to diffuse into urine as well. Meaning polyuria. This leads to dehydration causing polydipsia.
DM: signs and symptoms
Type 1: rapid onset of clinical triad over a few days
Polyuria, polydipsia and weight loss. may also be affected by other autoimmune diseases (such as coeliac, Grave’s Hashimotos)
Type 2: More gradual. Polyuria, Polydipsia, weight loss (though weight loss is v uncommon in type 2 compared to type 1). Blurred vision, lethargy and fatigue, genital thrush, recurrent infections
On exam: acanthosis nigracans (sign of insulin resistance), dyslipidaemia, high BP
DM: Investigations
Blood glucose. Random venous glucose Fasting venous glucose HbA1c >48. 42-48 - prediabetic. GOLD STANDARD: glucose tolerance test. ask patient to fast overnight, then give 75g of glucose. check after 2 hours Urinalysis
DM: Investigations
Blood glucose. Random venous glucose Fasting venous glucose HbA1c. >48 GOLD STANDARD: glucose tolerance test. ask patient to fast overnight, then give 75g of glucose. Urinalysis
DM: Fundoscopy
Background diabetic retinopathy
Dot and blot haemorrhages in retina
Pre- proliferative diabetic retinopathy
cotton wool spots (resulting from ischaemic damage caused by capillary occlusion)
Proliferative retinopathy
Neovascularisation, but these are more unstable so get haemorrhages
Advanced diabetic retinopathy
Recurrent vitreous hameorrahages
retinal detachment
DM: management. drugs (type 2)
1st line: metformin
impairs hepatic production of glucose and increases peripheral insulin sensitivity. SE: abdo pain, flatulence and diarrhoea/ constipation
ALTERNATIVES
gliptin
pioglitazone
sulfonylurea
SGLT-2i
2nd line:
Metformin + pioglitazone/ sulfonylurea/ SGLT- 2i
3rd line:
Triple therapy: metformin + gliptin/ pioglitazone +sulfonylurea
DM: Management. Lifestyle and education
Type 1: DAFNE
Type 2: DESMOND
CHD: Pathophysiology
foam cells (macrophages that have taken up LDLs) embed into the arterial wall damaged by HTN and form a plaque Stenosis of the LAD is ass w/ greater risk and poorer prognosis
CHD: Symptoms
Angina (chest tightness that can radiate to shoulder or arm)
Typical/ stable: bought on by physical exertion, fades quickly at rest
Decubitus: occurs when lying down (impaired LV function)
Prizmental’s: Coronary artery spasm at rest. More frequent in women, ST elavationd during pain
CHD: Investigations
QRisk2: assessment tool to calculate 1o year risk of developing CHD. Age, sex, ethnicity, location, smoking status, PMHx, FHX, BMI etc.
ECG: resting and exercise
Bloods: glucose, cholesterol
Echocardiogram
CHD: Management (1)
Lifestyle: Smoking, weight loss, dietry changes, exercise, stress management, DVLA: stop driving for 1 week if successful angioplasty, 4 weeks if unsuccessful angioplasty
CHD: Management (2) chronic
ACEi/ ARB for LV dysfunction, hypertension or diabetes
need to monitor renal function
B blocker: bisoprolol, this reduces myocardial oxygen demand
(can use a CCB if cannot use BB. in HF - amlodipine, in no HF- dilitiazem or verapamil)
Statin 80mg
Dual anti platelet therapy:
Aspirin
Ticagrelor
Surgery:
CABG- bypass
PCI - stent from an angioplasty
CHD: need to rule out
Need to rule out immediately life threatening:
Acute coronary syndrome
Pulmonary embolism
Aortic dissection
Tension pneumothorax
Spontaneous rupture of the oesophagus (Boerhaave’s syndrome)
CHD: Management
Need to rule out immediately life threatening:
Acute coronary syndrome
Pulmonary embolism
Aortic dissection
Tension pneumothorax
Spontaneous rupture of the oesophagus (Boerhaave’s syndrome)
Stroke: pathophysiology
disruption of blood supply to brain. Can either be as a result of ischeamia or haemorrhage.
Ischaemia- (80%). caused by embolus or thrombus formation. Can also by systemic hypoperfusion secondary to cardiac arrest.
Haemorrhagic- can get intracerebral, sub- arachnoid (usually due to burst berry aneurysm in circle of Willis)
Stroke: symptoms
sudden onset of CNS symptoms:
Stroke: diagnosis
sudden onset focal neuro symptoms from last 24 hrs. Confusion, headache (sudden/severe/ sentinel headaches in previous weeks), weakness in limbs, sensory loss, speech problems, visual problems, unilateral tongue weakness/ horner’s syndrome (ptosis, miosis and anhydrosis)
FAST can be used to screen: facial drooping, arm weakness, speech difficulty, time
Stroke: Management (chronic)
Lifestyle: smoking, alcohol, less salt, weight loss, exercise. Need to inform DVLA if problems after 1 month
Now treat RF—
antiplatelet- Clopidogrel for life (+PPI)
anticoag - Warfarin/ NOAC
Use Cha2DS2VASC score to assess risk of stroke
Use HASBLED to assess risk of bleed now on Anticoag
can also give anti-HTN meds: ACEi +diuretics
can also give statins
Inform DVLA.
Normal drivers if problems after a month
HGV- must inform
Stroke: Management (chronic)
Lifestyle: smoking, alcohol, less salt, weight loss, exercise. Need to inform DVLA if problems after 1 month
Now treat RF—
IF NO AF:
antiplatelet (aspirin, dipyramidole) - Clopidogrel for life (+PPI)
Statin
anticoag - Warfarin/ NOAC
Use Cha2DS2VASC score to assess risk of stroke (CHF (1), HTN (1), Age >75 (2), DM (1), stroke/TIA (2), Vascular disease (1), Age 65-74 (1), Sex- F (1)
Use HASBLED to assess risk of bleed now on Anticoag
(HTN (1), abnormal renal or liver function (1), stroke (1), Bleeding (1), Labile INR (1), Elderly (1), drugs or alcohol (1).
can also give anti-HTN meds: ACEi +diuretics
can also give statins
CKD: pathophysiology
GFR <60 mL/min for >3 MONTHS
also loss of hormonal function of kidneys.
All causes disturbance of electrolytes, increased BP and excess fluid
CKD: Aetiology
Vascular - HTN, renal artery stenosis, heart failure
Inflam/ infective- glomerulonephritis, pyelonephritis, interstitial nephritis
AI: SLE
Metabolic: DM (diabetic nephropathy - this is most common cause), renal stones, urinary tract obstruction, hypercalacaemia
Neoplastic: renal cancer
Envionment/ endocrine: parathyroid bone disease, malnutrition
CKD: symptoms
early: begins with generalised symptoms: tiredness, loss of appetite and headaches
Later: increased tiredness, paleness, headaches, visual disturbance, loss of appetite and nausea, pruritis, cafe-au-lait spots
final stages: renal failure leads to oliguria or anuria, dyspnoea, vomiting, bibasal crackles,
CKD: investigations
urinalysis: microalbuminuria (urine albumin: creatinine ratio), RBCs, glucose
Bloods: Uand Es, creatinine, eGFR, glucose, calcium, phosphate, protein, FBC, ESR, PTH
(GFR- measures how many ml of waste fluid kidneys can excrete per minute. Difficult to measure directly so is estimated to give eGFR. Estimate is based on lebel of creatinine and the patients demographics.
CKD, response:
lifestyle: smoking, alc, reduced sodium diet
Meds: stop all nephrotoxic drugs- NSAIDs, nicotine, aminoglycosides, X-ray contrast
Manage the risk factors by: HTN - ACEi/ARB
Hypercholesterloaemia: statin, clotting: antiplatelet
Hypertension: Pathophysiology
cardiac output remains the same but systemic resistance is increased. This is because large vessels show structural changes- deposition of calcium and increase in collagen.
LV hypertrophy. Reduced renal perfusion and greater GFR - may then activate the RAAS
Hypertension: Types
Essential - primary. Idiopathic
Secondary hypertension
renal disease - most common. Mostly due to renal disease like glomerulonephritis
endocrine - Cushing’s/ Conn’s (primary hyperaldosternoism)/ acromegaly
Malignant hypertension - URGENT. rapid rise in BP. 200/130/ Bilateral retinal haemorrhage and exudate
Hypertension: Symptoms
usually asymptomatic. On examination: tachycardia, a third heart sound and (if severe HTN) retinopathy
HTN: investigations
Ambulatory monitoring BP (over 24 hours)
ECG
Urine dip: test for protein and blood
Fasting blood for lipid profile
Fundoscopy -
Grad 1: subtle, generalised arteriolar narrowing
Grade 2: areas of focal narrowing, and compression of venules at sites of arteriovenous crossing (AV nipping)
Grade 3: development of features similar to diabetic retinopathy- retinal haemorrhages, hard exudates and cotton wool spots
Grade 4 (malingnant HTN): all features of grade 3 + optic disc swelling.
HTN: management
<55 >55 or black
A C
A+C
A+C+D
A+C+B
AF: Pathophysiology
Disorganised electrical activity in atria
Rapidly firing impulses cause disorganised depolarisation and ineffective atrial contraction.
AV node receives impulses more frequently than it can conduct so only some get through and results in irregular ventricular rhythm.
Atrial rhythm of 300-600 bpm, v. rhythm of 160-180
AF: symptoms
may cause palpatations, chest pain, dyspnoea, fatigue, light- headedness, syncope
Polyuria (found in all supraventricular arrhythmia like AF)
on exam: Tachycardic, irregular irregular pulse
AF: Investigations
ECG- absent p waves, irregular QRS complex. irregular RR intervals, chaotic baseline
Bloods: TFTs, FBC (anaemia), U and Es (infection), BNP (HF), cardiac enzymes (MI)
CXR- HF
AF: Management
First line - rate control (monotherapy). B Blocker (atenolol), CC-b (verapamil/ dilitiazem) (cannot give both BB and CCbas can casue AV block)
Digoxin
Second line: rhythm control.
<48 hrs- anticoagulation +rate/rhythm
>48 hrs- DC cardioversion (consider amiodarone 4 weeks before- 12 months after cardioversion)
AF: CHA2DS2VASC
CHF or LVSD (1), HTN (1), Age >75 (2), DM (1), Stroke/TIA/ thromboembolism (2), Vascular disease (1), Age 65-74 (1), sex(f) (1)
Consider Anticoag to anyone with score of 2 or above
Warfarin- Vit K antagonist.
NOACs (rivaroxaban) inhibits factor Xa. Less interactions and monitoring required
But monitor their HASBLED score for 1 year risk of major bleeding in patients anticoag w AF
COPD: pathophysiology
chronic bronchitis + emphysema. non reversible airway obstruction
Chronic bronchitis- inflammation of the bronchi
emphysema - damage to smaller airways and alveoli, loss of elasticity. leads to hyperinflated lungs
unlikely to develop in under 10 pack years
Pink Puffers
EmPhysema mostly
no CO2 retention - no cyanosis
reduced lung compliance, destruction of capillary bed . but as both ventilation and perfusion are reduced, there isn’t a V/Q mismatch. So no hypoxaemia
Body compensates by increased work of breathing
Normal/ low CO2 and normal O2
Pursed lips breathing maintains PEEP, tripod position
will develop heart disease and resp acidosis later than blue bloaters
Blue Bloaters
Chronic Bronchitis
Will get air trapping and retain CO2
Obstruction leads to decreased ventillation but normal perfusion, so VQ mismatch = hypoxaemia.
Fail to maintain resp. effort so high CO2 and low O2
patients become reliant on hypoxaemic drive, not on CO2 levels
Get pulmonary hypertension, to try and cope with VQ mismatch
This can lead to RSHF- cor pulmonale
COPD: Symptoms
productive cough, white or clear sputum EXPIRATORY wheeze (if insp then it is an exacerbation) SOB No pain/ blood OE: barrel chested- hyperinflated SOB at rest accessory muscles for breathing pursed lip breathing Coarse crackles, prolonged exp. phase
COPD: complications
Resp infections:
Haem. influenzae
Moraxella catarrhalis
Strep. pneumoniae
sputum changes colour to yellow/green
increased in SOB
pleuritic pain
COPD: Investigations
MRC dyspnoea scale (3- walks slower than others, 4- SOB at 100m, 5- too SOB to leave house) Spirometry FEV1 <80% of predicted FVC normal or slightly reduced FEV1/ FVC <0.7 Serum alpha 1 antitrypsin -
COPD: treatment chronic
- SABA and SAMA (iprotropium)
- LABA (salmeterol) and LAMA (tiotropium)
- ICS and LABA
- Triple therapy- LABA + LAMA+ ICS
COPD: treatment acute
CO: controlled oxygen:venturi
S: Salbutamol 5mg NEB
I: Ipratropium 0.5mg NEB
C: corticosteroids- prednisolone 30 mg PO/ Hyrdocortisone 200 mg IV
A: Abx +aminophylline (similar to theophylline)
R:Radiotherapy (CXR) + Resp support (BiPAP if high CO2)
profilcaxis for osteoporosis (as corticosteroid induced and due to catabolic mechanisms due to increased work of breathing) - Calcium and vit D3
Stroke: management (acute)
If ischaemic: thrombolysis with alteplase and aspirin for 2 weeks
If haemorrhagic: prothrombin and Vit K to nromalise clotting
