GP ILAs Flashcards
1
Q
What is needed to confirm a diagnosis of Hypertension
A
24hr ABPM or a week of at home readings
2
Q
At what BP reading should treatment be offered
A
all with BP ≥160/100mmHg or ABPM ≥150/95mmHg.
3
Q
Health conditions which can cause hypertension
A
- Kidney disease/long term infections
- Diabetes
- Glomerulonephritis
- Hormone issues- underactive thyroid, Cushing’s, Acromegaly, hyperaldosteronism, phaechromocytoma
4
Q
Medications which can cause hypertension
A
- contraceptives
- steroids
- NSAIDs
- Cocaine/amphetamines
- Some SSNRIs e.g. venlafaxine
5
Q
How can hypertension affect the kidney?
A
○ People with hypertension and normal kidney function have a significantly reduced number of nephrons in each kidney
○ Individual nephrons are enlarged as a result of glomerular hyperfiltration
6
Q
what tests are used to quantify overall risk of a hypertension diagnosis?
A
fasting glucose and cholesterol
7
Q
what tests are used to look for end-organ damage from hypertension
A
- ECG/Echo (LVH or history of MI?)
- Urine analysis (protein, blood)
8
Q
What test can exclude secondary causes of hypertension
A
Bloods- U&E: decreased K+ in Conn’s, increased Ca2+ in hyperparathyroidism
9
Q
Explain pathophysiology of essential hypertension
A
Primary (essential hypertension): arteriosclerosis of major renal arteries, and changes in intrarenal vasculature (nephrosclerosis)
- blood vessel wall becomes hyalinised in small vessels and arterioles as the intima thickens with reduplication of the internal elastic lamina
- Concentric reduplication of internal elastic lamina and endothelial proliferation lead to ‘onion skin’ appearance
- both kidneys reduce in size- can be asymmetrical if one major vessel is affected
- proportion of sclerotic (scarred) glomeruli increases
10
Q
What is the range for stage 1 Hypertension
A
a systolic BP of 130-139 or a diastolic BP of 80-89
11
Q
What is the range for stage 2 hypertension
A
systolic>140, diastolic>90
12
Q
is the cause of essential (primary) hypertension known or unknown?
A
unknown
13
Q
what percentage of hypertension cases are secondary hypertension and what is secondary hypertension?
A
5% . Secondary Hypertension= Hypertension with an identifiable cause i.e. secondary to another condition.
14
Q
what are some causes of secondary hypertension?
A
- renal disease (intrinsic issues such as glomerulonephritis, systemic sclerosis and PCKD & renovascular diseases which are usually atheromatous)
- Endocrine disease e.g. Cushing’s, Conn’s, Phaechromocytoma, Acromegaly, Hyperparathyroidism
- coarctation, pregnancy, drugs (steroids, oral contraceptive, cocaine, amphetamines)
15
Q
Treatment pathway for a patient with type 2 diabetes diagnosed with hypertension? (4 steps)
A
(1) ACEi/ARB
(2) (ACEi/ARB) + CCB/thiazide-like diuretic
(3) ACEi/ARB + CCB + thiazide-like diuretic
(4) Confirm resistant hypertension and consider seeking expert advice or adding a low-dose spironolactone if blood potassium level is ≤4.5mmol/l OR an alpha-blocker/beta-blocker if potassium level is >4.5mmol/l
16
Q
Treatment pathway for patient <55, not of black/afro-Caribbean descent and with no diabetes who is diagnosed with hypertension? (4 steps)
A
(1) ACEi/ARB
(2) (ACEi/ARB) + CCB/thiazide-like diuretic
(3) ACEi/ARB + CCB + thiazide-like diuretic
(4) Confirm resistant hypertension and consider seeking expert advice or adding a low-dose spironolactone if blood potassium level is ≤4.5mmol/l OR an alpha-blocker/beta-blocker if potassium level is >4.5mmol/l
17
Q
Treatment pathway for patient age 55 or over with no diabetes?
A
(1) CCB
(2) (CCB) + ACEi/ARB/thiazide-like diuretic
(3) ACEi/ARB + CCB + thiazide-like diuretic
(4) Confirm resistant hypertension and consider seeking expert advice or adding a low-dose spironolactone if blood potassium level is ≤4.5mmol/l OR an alpha-blocker/beta-blocker if potassium level is >4.5mmol/l
18
Q
Hypertension treatment algorithm for patient with black african or afro-caribbean family origin (any age)?
A
(1) CCB
(2) (CCB) + ACEi/ARB/thiazide-like diuretic
(3) ACEi/ARB + CCB + thiazide-like diuretic
(4) Confirm resistant hypertension and consider seeking expert advice or adding a low-dose spironolactone if blood potassium level is ≤4.5mmol/l OR an alpha-blocker/beta-blocker if potassium level is >4.5mmol/l
19
Q
How often should patients with hypertension be monitored:
1- adjusting their hypertension medication
2-once stabilised
3- serum potassium and creatinine
A
1- when adjusting medication BP should be monitored every 2-4 weeks
2- Once stabilised, BP should be checked and medications reviewed every 6-12 months
3- Serum Potassium and Creatinine should be checked yearly
20
Q
What are the 3 most likely complications of hypertension?
A
Coronary artery disease, cerebrovascular accidents (e.g. stroke) and Left Ventricular Hypertrophy
21
Q
hypertension medications which can result in erectile dysfunction
A
thiazide-like diuretics and beta blockers
22
Q
hypertension medication which results in ankle swelling
A
calcium channel blockers
23
Q
hypertension medications which result in dry cough
A
ACE inhibitors e.g. ramipril
24
Q
Most common cause of HF in the developed world
A
Ischaemic heart disease
25
Pathophysiology of HF (3 basic steps)
1- initial stressful event (e.g. infarction/inflammation/pressure or volume overload) leads to myocardial damage which causes increased myocardial wall stress. This results in initial HF
2- compensatory mechanisms are activated which attempt to maintain cardiac output snd peripheral perfusion. As HF progresses, these are overwhelmed. These include the RAAS, sympathetic nervous system, ventricular dilatation/remodelling and release of cytokines e.g. TNF
3-The compensatory physiological changes become pathological and damaging; All of this leads to further wall stress- vicious cycle
26
Explain the RAAS role in hypertension
(1) Renin (enzyme) released from granular cells of the renal juxtaglomerular apparatus in response to (i) reduced sodium delivery to distal convoluted tubule detected by macula densa cells, (ii) reduced perfusion pressure in the kidney detected by baroreceptors in the afferent arteriole and (iii) sympathetic stimulation of the JGA via B1 adrenoreceptors. Renin release is inhibited by ANP which is released by stretched atria in response to increases in BP
(2) Angiotensinogen (produced in the liver) is cleaved by renin to form Angiotensin I
(3) Angiotensin I is converted to Angiotensin II by ACE (angiotensin converting enzyme)
(4) Angiotensin II stimulates the release of Aldosterone from the adrenal cortex. Aldosterone acts on the principal cells of the collecting ducts in the nephron, increasing expression of ENaC to reabsorb urinary sodium, and increase the activity of basolateral Na/K/ATPase is increased. This increases sodium reabsorption of urinary sodium. In exchange, potassium is moved from the blood into the principal cell of the nephron and exits the cell into the renal tubule to be excreted into the urine.
27
Actions of Angiotensin II (4)
(1) stimulates release of Aldosterone
(2) cardiovascular- acts on AT1 receptors in endothelium of arterioles throughout the circulation to achieve vasoconstriction, resulting in an increase in TPR and consequently BP
(3) Neural effects: acts at hypothalamus to stimulate the sensation of thirst, resulting in an increase in fluid consumption, which helps raise the circulating volume and in turn the BP. Also increases secretion of ADH from the posterior pituitary gland, which results in the production of more concentrated urine to reduce the loss of fluid from urination. This allows circulating volume to be better maintained until more fluids can be consumed. Also stimulates the sympathetic nervous system to increase release of noradrenaline which is typically associated with fight or flight and increases CO, vasoconstricts arterioles and releases renin
(4) Renal effects: acts on kidney to produce a variety of effects including afferent and efferent arteriole constriction and increased Na+ reabsorption in the proximal convoluted tubule
28
most likely pathological heart sound for heart failure
S3 sound
29
risk factors for HF
hypertension, ischaemic heart disease, smoking, alcohol, obesity, (possibly diabetes?), sedentary lifestyle
30
main causes of RVF
LVF
Tricuspid valve disease
cor pulmonalae
31
Left ventricular systolic dysfunction (LVSD) is also known as
heart failure with reduced ejection fraction. Commonly caused by ischaemic heart disease but can also occur with valvular heart disease and hypertension
32
causes of right ventricular systolic dysfunction
left ventricular systolic dysfunction, primary and secondary pulmonary hypertension, right ventricular infarction, adult congenital heart disease
33
diastolic heart failure is also known as
heart failure with normal ejection fraction. Where the patient has symptoms and signs of heart failure with a normal or near-normal left ventricular ejection fraction (45-50%) and evidence of diastolic dysfunction on echo (e.g. abnormal left ventricular relaxation and filling, usually with left ventricular hypertrophy). This leads to impairment of diastolic ventricular filling and hence decreased cardiac output. Diastolic failure is more common in elderly hypertensive patients but may occur with cardiomyopathy.
34
presentation- left sided heart failure
- paroxysmal nocturnal dyspnoea
- restlessness
- orthopnoea (SOB when lying flat)
- dyspnoea (on exertion or at rest)
- elevated pulmonary capillary wedge pressure
- tachycardia
- fatigue
- cyanosis
- pulmonary congestion (cough, crackles, wheeze, blood-tinged sputum, tachypnoea)
35
presentation- right sided heart failure (cor pulmonale)
- fatigue
- increased peripheral venous pressure
- ascites
- hepatomegaly/splenomegaly
- may be secondary to chronic pulmonary problems
- distended jugular veins
- anorexia/complaints of GI distress
- weight gain
- pitting oedema/leg swelling
36
NYHA classification of heart failure- Class I
no limitation. Normal physical exercise does not cause fatigue, dyspnoea or palpitations
37
NYHA classification of heart failure- Class II
mild limitation. Comfortable at rest but normal physical activity produces fatigue, dyspnoea or palpitations
38
NYHA classification of heart failure- Class III
Marked limitation. Comfortable at rest but less gentle physical activity produces marked symptoms of heart failur
39
NYHA classification of heart failure- Class IV
symptoms of HF occur at rest and are exacerbated by any physical activity
40
first line investigation for chronic HF
NT-proBNP (released when the myocardial tissue is stretched). if suspected HF would also want to do an ECG and consider CXR + urinalysis + spirometry
41
if a suspected chronic HF patient has a NT-proBNP >2000 ng/l, you should
refer urgently (2ww) to be seen by cardiology for a transthoracic echo
42
If a suspected chronic HF patient has NT-proBNP between 400-2000 ng/l, you should
refer urgently to be seen within 6 weeks by cardiology for transthoracic echo
43
If suspected chronic HF patient has NT-proBNP <400 ng/l, this means
you should consider other causes of symptoms as HF is not confirmed
44
suspected acute HF should be ruled out/confirmed by
taking a single measurement of BNP or NT-proBNP and HF should be ruled out if BNP<100ng/l or NT-proBNP <300ng/l. If does meet threshold, next step is transthoracic echo
45
Chronic HF management- pharmacology
Symptomatic relief: diuretics for congestive symptoms/fluid retention
- 1st line: ACEi + beta blocker
- 2nd line: Aldosterone antagonist(e.g/ spironolactone)/ARBs/Hydralazine (particularly if African) + nitrate eg isosorbide dinitrate
- 3rd line: cardiac resynchronisation therapy (biventricular pacemaker) OR digoxin (strongly recommended if coexistent Afib). Alternative to digoxin is ivabradine (but should only be used for patient with heart rate >75)
46
which vaccination do HF patients need annually?
influenza
47
which HF treatment drugs increase lifespan (reduce mortality)
beta blockers, ACEIs, spironolactone. (furosemide treats symptoms but does not increase life span)
48
ACE Inhibitor mechanism of action
inhibits production of angiotensin II (blocks conversion from angiotensin I to II), a potent vasoconstrictor and increases concentration of vasodilator bradykinin. thereby increases renal salt and water excretion and increases cardiac output by reducing afterload.
49
drugs which can cause first dose hypotension
ACE Inhibitors
50
isosorbide mononitrate- drug class? when is it used?
vasodilator. Used in combination with hydralazine if patients are intolerant of ACEIs/ARBs (especially if Afro-Caribbean)
51
Acute management- HF with systolic dysfunction
(1) High flow oxygen. CPAP sometimes indicated. Furosemide iv e.g. 50mg
(2) Clinical evaluation and systolic BP
- SBP>100: Give vasodilator e.g. GTN, nitroprusside, BNP
-SBP 85-100: Vasodilator and/or inotropic (dobutamine, PDEI)
· SBP<85:
Volume loading? Inotropic and/or dopamine and/or noradrenaline
(3) No response to initial treatment: consider mechanical assist devices e.g. right or left ventricular assist devices
(4)
When a good response is established: oral therapy, furosemide, ACEI
52
Can the MMR vaccination be given to pregnant women
MMR vaccines should not be administered to women known to be pregnant or attempting to become pregnant; to avoid becoming pregnant for 28 days after receipt of MMR vaccine (CDC 2013)
53
3 steps of assessing fever in an under 5y/o
1- identify any immediately life-threatening features, including compromise of the airway/breathing/circulation and decreased level of consciousness. Could this be sepsis?
2- use traffic light system to predict risk of serious illness
3- assess for specific illnesses
54
Traffic light system (Children): Red light (high risk) factors for children
- colour: pale/mottled/ashen/blue
- activity: no response to social cues, appears ill, does not wake or if roused does not stay awake, weak, high pitched/continuous cry
- respiratory: grunting, tachypnoea, RR>60 breaths/min, moderate/severe chest indrawing
- reduced skin turgour
- non-blanching rash, bulging fontanelle, neck stiffness, temp 38 or above in children < 3 months, focal neurological signs/status epilepticus/focal seizures
55
If there are any red features suggesting a serious or life-threatening cause of febrile illness such as sepsis or central nervous system infection, you should
arrange emergency ambulance transfer to Accident and Emergency
56
Traffic light system (children): If there are any other non life-threatening red features...
an urgent face-to-face assessment within 2 hours should be arranged if the infant or child was initially assessed by telephone, to help guide whether urgent hospital admission is needed.
57
Traffic light system (children): If there are any amber features (but no red features)
a face-to-face assessment should be arranged if the infant or child was initially assessed by telephone, the urgency depending on clinical judgement, to help guide whether hospital admission is needed or whether the child can be managed at home.
58
Traffic light system (children): if there are green features (but no amber/red features),
the child can usually be managed at home, including:
- Assessing for and managing any underlying cause of fever such as urinary tract infection, if appropriate.
- Advising on the use of paracetamol or ibuprofen to reduce fever if the child is uncomfortable or distressed, and on measures to prevent dehydration.
- Providing advice on sources of information and support.
- Providing the parents/carers with safety netting advice on warning symptoms and signs and when medical review is needed.
59
Traffic light system (Children): Amber (intermediate risk) factors
- Colour: pallor reported by parent/carer
- Activity: not responding normally to social cues, no smile, wakes only with prolonged stimulation, decreased activity
- respiratory: nasal flaring, tachypnoea (RR>50 breaths/min if age 6-12 months, RR>40 breaths/min if age >12 months), oxygen saturation <95% in air, crackles in chest
- circulation/hydration: Tachycardia: >160 beats/min if less than 1, >150 beats/min age 1-2, >140 beats min age 2-5yrs; CRT >3 secs, dry mucous membranes, poor feeding in infants, reduced urine output
- misc: age 3-6 months, temp 39 degrees or more, fever for 5 days or more, rigors, swelling of limb/joint, non-weight bearing limb/not using an extremity, capillary refill time of 3 seconds or longer
60
children with a fever of 5 days or more should be assessed for
Kawasaki disease
61
Signs of dehydration in children include
- prolonged capillary refill time
- Abnormal skin turgour
- Abnormal respiratory pattern
- Weak pulse
- Cool extremities
62
Meningococcal disease presentation in children
- lesions larger than 2mm in diameter (purpura)
- capillary refill time of 3 seconds or longer
- neck stiffness
63
Bacterial meningitis presentation in children
- neck stiffness
- bulging fontanelle
- decreased level of consciousness
- convulsive status epilepticus
64
herpes simplex encephalitis presentation in children
consider herpes simplex encephalitis in children with fever and any of the following features:
- focal neurological signs
- focal seizures
- decreased level of consciousness
65
pneumonia presentation in children
- tachypnoea
- crackles in the chest
- nasal flaring
- chest indrawing
- cyanosis
- oxygen saturation of 95% or less when breathing air
66
UTI presentation in children
- Consider UTI in any child younger than 3 months with a fever
- Consider UTI in a child aged 3 months or older with fever and 1 or more of the following: vomiting, poor feeding, lethargy, irritability, abdominal pain/tenderness, urinary frequency/dysuria
67
Septic Arthritis/Osteomyelitis presentation
consider septic arthritis/osteomyelitis in children with fever and any of the following signs:
- swelling of a limb or joint
- not using an extremity
- non-weight bearing
68
Kawasaki disease presentation
Consider Kawasaki disease if CRASH & Burn:
Conjunctivitis- non exudative, bilateral infection
Rash- nonvesicular, no bullae. Erythmatous, maculopapular, mobilliform
Adenopathy- cervical, unilateral
Strawberry tongue- redness of oral mucosa, lips or dry peeling lips
Hands- swelling or erythema of hands or feet
+ Burn (fever of 5 days or more)
69
FeverPAIN score criteria (5)
- fever (during last 24hrs)
- purulence (pus on tonsils)
- attend rapidly (within 3 days after onset of symptoms)
- severely inflamed tonsils
- no cough or coryza (inflammation of mucus membranes in the nose)
70
likelihood of isolating streptococcus with a FeverPAIN score of 0-1
13-18%
71
likelihood of isolating streptococcus with a FeverPAIN score of 2-3
34-40% (could give delayed script antibiotics)
72
likelihood of isolating streptococcus with a FeverPAIN score of 4-5
62-65% (give antibiotics)
73
Centor criteria (4) + interpretation of results
- presence of tonsillar exudate
- tender anterior cervical lymphadenopathy/lymphadenitis
- history of fever
- absence of cough
score of 0,1 or 2= 3-17% likelihood of isolating streptococci; 3-4= 32-56% chance of isolating streptococci
74
Treatment for streptococcal infection
phenoxymethylpenicillin, or erythromycin if patient is allergic to penicillin. Should be given for 7-10 days
75
MMR doses are given at
first dose at 12 months, second dose at 3-5 years
76
measles causative organism + method of spread
RNA paramyxovirus, spread by droplets
77
incubation period for measles
10-14 days
78
when is measles infectious?
from prodrome (fever/malaise + 3 Cs: cough, coryza, conjunctivitis) until 4 days after the rash starts
79
mouth sign seen in measles
Koplik spots- white spots on buccal mucosa like 'grains of salt'
80
rash in measles- characteristics
discrete, maculopapular rash initially, spreads from behind the ears to the whole body. Becomes blotchy and confluent. May desquamate in the second week
81
investigation for Measles
IgM antibodies can be detected within a few days of rash onset
82
Measles treatment
- supportive
- children admitted to hospital should be isolated
- in immunocompromised patients, antiviral drug ribavirin may be used
- notifiable disease so notify public health
83
What antibiotic medication used to treat UTIs is contraindicated when taking methotrexate and when might methotrexate be used
Trimethoprim, methotrexate may be used to treat rheumatoid arthritis
84
difference between the distribution of eczema and psoriasis
eczema= flexor surfaces (elbow crease + knee crease), psoriasis= on extensors (elbow and knee )
