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GP core conditions Flashcards

1
Q

Asthma: patho physiology

A

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

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2
Q

asthma: symptoms

A

Clinical triad:
• Dry chronic cough (worse at night)
• SOB
• Expiratory wheeze

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3
Q

asthma: acute signs

A 
Acute signs:
•	Tachypnoea 
•	Expiratory wheeze 
•	Hyperinflated chest
•	PEFR <33%
•	Paradoxical pulse (bp falls on inspiration)
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4
Q

Asthma:Investigations

A

spirometry: FEV1/ FVC < 70%

you can perform an FEV1 reversibility test

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5
Q

Asthma: Management

Under 5s

A
  1. Short acting B2 agonist
  2. +Regular low dose inhaled corticosteroid (ICS) for 8 weeks)
  3. +LTRA (leukotriene receptor antagonist) (montelukast)
  4. Increase dose of steroids
  5. Oral steroids
  6. Refer
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6
Q

Asthma: Management

Over 5s

A
  1. SABA (salbutamol or terbutaline)
  2. ICS (beclometasone or fluticasone) +oral LTRA
  3. ICS +inhaled LABA (salmeterol)
  4. Moderate dose ICS +LABA
  5. High dose ICS
  6. Add theophylline
  7. Oral steroids (prednisolone) + refer
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7
Q

Heart Failure: pathophysiology

A

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
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8
Q

Heart failure: Symptoms

A 
Cough (esp at night). pink frothy sputum
PND
decreased exercise tolerance
SOB
sweating and clammy
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9
Q

Heart failure: signs

A 
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
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10
Q

Heart failure: Diagnosis

A

gold standard: use echocardiogram – measures Ejection fractions
in GP- BNP (relates to damaged heart muscle)
Framlingham criteria
New York Hear Association classification

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11
Q

Heart failure: investigation (1)

A

Echo
ECG
Chest X- ray
Bloods

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12
Q

Heart failure: investigations (2)

A

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

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13
Q

HF, Management: acute

A

Oxygen
Morphine
Furosemide - 40-80 mg IV
GTN spray - vasodilator (if compensating HF, refer to senior to not tip person into cardiogenic shock)

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14
Q

HF, management: chronic

A

Diuretics: FUROSEMIDE, spironolactone
ACEi - lisinopril/ ramipril
B BLOCKER - bisoprolol
digoxin - decreases heart rate and increases heart contractility

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15
Q

Diabetes Mellitus: Pathophysiology (1)

A

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.

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16
Q

DM: Pathophysiology (2)

A

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.

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17
Q

DM: signs and symptoms

A

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

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18
Q

DM: Investigations

A 
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
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19
Q

DM: Investigations

A 
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
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20
Q

DM: Fundoscopy

A

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

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21
Q

DM: management. drugs (type 2)

A

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

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22
Q

DM: Management. Lifestyle and education

A

Type 1: DAFNE

Type 2: DESMOND

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23
Q

CHD: Pathophysiology

A 
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
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24
Q

CHD: Symptoms

A

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

25
Q

CHD: Investigations

A

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

26
Q

CHD: Management (1)

A

Lifestyle: Smoking, weight loss, dietry changes, exercise, stress management, DVLA: stop driving for 1 week if successful angioplasty, 4 weeks if unsuccessful angioplasty

27
Q

CHD: Management (2) chronic

A

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

28
Q

CHD: need to rule out

A

Need to rule out immediately life threatening:
Acute coronary syndrome

Pulmonary embolism

Aortic dissection

Tension pneumothorax

Spontaneous rupture of the oesophagus (Boerhaave’s syndrome)

29
Q

CHD: Management

A

Need to rule out immediately life threatening:
Acute coronary syndrome

Pulmonary embolism

Aortic dissection

Tension pneumothorax

Spontaneous rupture of the oesophagus (Boerhaave’s syndrome)

30
Q

Stroke: pathophysiology

A

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)

31
Q

Stroke: symptoms

A

sudden onset of CNS symptoms:

32
Q

Stroke: diagnosis

A

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

33
Q

Stroke: Management (chronic)

A

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

34
Q

Stroke: Management (chronic)

A

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

35
Q

CKD: pathophysiology

A

GFR <60 mL/min for >3 MONTHS
also loss of hormonal function of kidneys.
All causes disturbance of electrolytes, increased BP and excess fluid

36
Q

CKD: Aetiology

A

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

37
Q

CKD: symptoms

A

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,

38
Q

CKD: investigations

A

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.

39
Q

CKD, response:

A

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

40
Q

Hypertension: Pathophysiology

A

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

41
Q

Hypertension: Types

A

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

42
Q

Hypertension: Symptoms

A

usually asymptomatic. On examination: tachycardia, a third heart sound and (if severe HTN) retinopathy

43
Q

HTN: investigations

A

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.

44
Q

HTN: management

A

<55 >55 or black
A C
A+C
A+C+D
A+C+B

45
Q

AF: Pathophysiology

A

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

46
Q

AF: symptoms

A

may cause palpatations, chest pain, dyspnoea, fatigue, light- headedness, syncope
Polyuria (found in all supraventricular arrhythmia like AF)
on exam: Tachycardic, irregular irregular pulse

47
Q

AF: Investigations

A

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

48
Q

AF: Management

A

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)

49
Q

AF: CHA2DS2VASC

A

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

50
Q

COPD: pathophysiology

A

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

51
Q

Pink Puffers

A

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

52
Q

Blue Bloaters

A

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

53
Q

COPD: Symptoms

A 
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
54
Q

COPD: complications

A

Resp infections:
Haem. influenzae
Moraxella catarrhalis
Strep. pneumoniae

sputum changes colour to yellow/green
increased in SOB
pleuritic pain

55
Q

COPD: Investigations

A 
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 -
56
Q

COPD: treatment chronic

A
  1. SABA and SAMA (iprotropium)
  2. LABA (salmeterol) and LAMA (tiotropium)
  3. ICS and LABA
  4. Triple therapy- LABA + LAMA+ ICS
57
Q

COPD: treatment acute

A

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

58
Q

Stroke: management (acute)

A

If ischaemic: thrombolysis with alteplase and aspirin for 2 weeks
If haemorrhagic: prothrombin and Vit K to nromalise clotting

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