Wednesday [12/4/23]

Question 1

how to interpet BBBaaa

Answer 1

aaa

Question 2

reading ECGs

Answer 2

a

Question 3

What is EPO and how does it work?

Answer 3

Erythropoietin, also known as erythropoetin, haematopoietin, or haemopoietin, is a glycoprotein cytokine secreted mainly by the kidneys in response to cellular hypoxia; it stimulates red blood cell production in the bone marrow

Question 4

how much of ferrous fumarate is absorbed? [1]
bisphosphonates ad surgery

Answer 4

typically 10% of th eingested dose is absorbed, however the proportion is highly vairbale, and is a function of iron stores and ingested dose

Question 5

reading CXR

Answer 5

a

Question 6

What is primary hyperparathyroidism? [1]

Answer 6

Increased parathyroid hormone which causes excess calcium . Occurs in the parathyroid gland.

Question 7

commonest population affected by it? [1]

Answer 7

women and elderly

Question 8

Causes of primary hyperparathyroidism [4]

Answer 8

Aetiology
85%: solitary adenoma
10%: hyperplasia
4%: multiple adenoma
1%: carcinoma

Question 9

How often is the inherited form of hyperparathyroidism? Name these conditions [3]

Answer 9

These inherited forms occur in approximately 15% of cases. Inherited disorders responsible for primary hyperparathyroidism include:
Multiple endocrine neoplasia (MEN)
Hyperparathyroidism jaw tumour syndrome
Familial isolated primary hyperparathyroidisma

Question 10

what is normal calcium regulation? [4]

Answer 10

Reduced serum calcium → PTH secretion by the parathyroid gland → PTH binds to receptors within the bones and kidneys → calcium is moved from the bones and kidneys into the bloodstream → calcium re-enters the normal range → PTH levels drop.

Question 11

How does primary hyperparathyroidism disrupt calcium homeostasis?

Answer 11

However, in primary hyperparathyroidism a region of cells within the parathyroid glands cease to respond to this negative feedback loop. These cells continuously secrete PTH irrespective of the serum calcium concentration. This results in hypercalcaemia.
Over time, the region of cells secreting excess parathyroid hormone grows and the levels of PTH and therefore calcium slowly rise.
As the hypercalcaemia worsens the patient will begin to develop symptoms.

Question 12

most common Sx of primary hyperparathyroidism? [1]

Answer 12

aSx

Question 13

other features of high calcium, including serious presentations [4]

Answer 13

Other features include polyuria, paresthesia and muscle cramps. As calcium levels rise more serious symptoms develop. In severe cases, cardiac and metabolic disturbances, delirium or even coma may occur. The history should also screen for symptoms of malignancies, including but not limited to unexplained weight loss, night sweats and pain.a

Question 13

Other Sx of 1 PTH [4]

Answer 13

stones, bones, abdominal groans, psychiatric overtones

Question 14

What should Ca and PTH be in primary PTH? exception to the rule? [2]

Answer 14

Typically, both calcium and PTH should be raised, although a raised serum calcium and a normal PTH is also indicative of primary hyperparathyroidism. This is because the PTH levels are inappropriately high in the context of a raised calcium.a

Question 15

Which Ix should be done to r/o FHH? [1]

Answer 15

Findings of raised serum adjusted calcium and PTH indicate the presence of a parathyroid-dependant hypercalcaemia. This limits the cause to a small number of conditions. To differentiate these the following investigations should be considered:
24-hour urinary calcium to exclude familial hypocalciuric hypercalcaemia
High-normal in primary hyperparathyroidism, but low in familial hypocalciuric hypercalcaemia

Question 16

Additional Ix to do in primary PTH [4]

Answer 16

Estimated glomerular filtration rate (eGFR) and creatinine to assess hydration status, risk of acute kidney injury and presence of chronic kidney disease
Serum and urine protein electrophoresis, including testing for urine Bence-Jones protein to exclude myeloma
Full blood count (FBC) to exclude haematological malignancy
Liver function tests (LFTs) to exclude liver metastasis and some systematic diseases
Dual energy x-ray absorptiometry (DEXA) to assess bone health and risk of osteopenia/osteoporosis

Imaging may be indicated to identify lesion if a surgical intervention is desired. The most commonly used imaging used in primary hyperparathyroidism is ultrasound, but CT and MRI are sometimes indicated.

Question 17

What is an important differential in hyperacalcaemia? [2]

Answer 17

Malignancy is the most common differential and therefore should be excluded in all patients. Hypercalcaemia of malignancy has 2 main mechanisms:
PTH-related-protein (PTHrP) secreting tumours (e.g. lung, breast and kidney)
Osteolytic lesions (e.g. bone metastasis and multiple myeloma)

Question 18

How to differentiate between malignancy and hyperparathyroidism? [1]

Answer 18

serum PTH is low in hypercalcaemia of malignancy

Question 19

What is FHH? [2]

Answer 19

Familial hypocalciuric hypercalcaemia (FHH) is a rare autosomal domination condition in which there is reduced renal excretion of calcium. Patients are asymptomatic and are characterised by raised serum adjusted calcium and normal-raised PTH levels similar to primary hyperparathyroidism. These patients generally do not require treatment, so differentiation from primary hyperparathyroidism is important.
Differentiated with a 24-hour urinary calcium
FHH results in a hypocalciuria
Primary hyperparathyroidism results in high or normal urinary calcium
A diagnosis of FHH can be confirmed with genetic testing

Question 20

Indication for surgery according to 2019 guidelines? 4

Answer 20

Surgery is indicated for those with one or more of:
Symptomatic disease
Symptoms of hypercalcaemia
Osteoporosis and/or fragility fractures
Renal stones or nephrocalcinosis
Age <50 years
Serum adjusted calcium of 2.85 mmol/L or above
Estimated glomerular filtration rate (eGFR) of less than 60 mL/min/1.73 m²

Question 21

Cure rate with parathyroidectomy [1]

Answer 21

98%

Question 22

When surgery not an option for patients what can be given? [1]

Answer 22

Calcitonin which reduces serum calcium concentrations by inhibiting bone and kidney resorption of calcium
Cinacalcet which is a calcimimetic and acts to reduce serum calcium concentrations while not affecting bone density or urinary calcium concentrations
Desunomab which also impairs calcium resorption
Bisphosphonatesa

Question 23

When surgery not an option for patients what can be given? [1]

Answer 23

aCalcitonin which reduces serum calcium concentrations by inhibiting bone and kidney resorption of calcium
Cinacalcet which is a calcimimetic and acts to reduce serum calcium concentrations while not affecting bone density or urinary calcium concentrations
Desunomab which also impairs calcium resorption
Bisphosphonates

Question 24

Cx of untreated PPTH

Answer 24

Osteoporosis and fragility fractures
Kidney stones and kidney injury
Hypertension and heart disease
Numerous gastrointestinal disorders including peptic ulcer disease, pancreatitis and gall stones

Question 25

Cx of parathyroidectomy [4]

Answer 25

General surgical complications (reduced risk with good surgical practice)
Infection
Thrombosis
Scarring
Procedure specific complications
Damage to the recurrent or superior laryngeal nerves
Post operative hypocalcaemia can result after the removal of too much parathyroid tissue
Failure to identify adenoma or persistence of disease post-surgery

Question 26

Difference between primary and secondary hyperparathyroidism

Answer 26

This occurs from a disorder either within the parathyroid glands (primary hyperparathyroidism) or as response to external stimuli (secondary hyperparathyroidism)

Question 27

What is the most common Sx with long-standing hyhperparathyroidism? [1]

Answer 27

kidney stones

Question 28

what is secondary hyperparathyroidism due to? [3]

Answer 28

vitamin D deficiency, chronic kidney disease,

Question 29

when does secondary hyparathyroidism happen? [1]

Answer 29

when calcium level abormally low

Question 30

tertiary hyperparathyroidism biochemistry

Answer 30

tertiary hyperparathyroidism has a high PTH and high serum calcium

Question 31

when does tertiary hyperparathyroidism occur? [2]

Answer 31

Tertiary hyperparathyroidism is seen in those with long-term secondary hyperparathyroidism, which eventually leads to hyperplasia of the parathyroid glands and a loss of response to serum calcium levels. This disorder is most often seen in patients with end-stage kidney disease and is an autonomous activity

Question 32

what proportion of the world anaemic? [1]

Answer 32

more than 1/4, with more than half from IDA

Question 33

why theortically, does IV iron work more than PO? [2]

Answer 33

when does tertiary hyperparathyroidism occur? [2]

Question 34

why theortically, does IV iron work more than PO? [2]

Answer 34

when does tertiary hyperparathyroidism occur? [2]a

Question 35

what does 1 small square = ECG? [1]

Answer 35

0.04s

Question 36

what does 1 large square equal ecg? [1]

Answer 36

0.20s

Question 37

calculating rate ECG

Answer 37

300 divided by large squares, or 1500 divided by small squares, or number of R waves x6 rhyhtm strip if 10s long

Question 38

QRS morphology narrow complex vs wide complex [2]

Answer 38

Narrow complex: sinus, atrial or junctional origin.

Wide complex: ventricular origin, or supraventricular with aberrant conduction.

Question 39

narrow complex type of rhythms

Answer 39

Sinus tachycardia
Atrial tachycardia
Atrial flutter
Inappropriate sinus tachycardia
Sinus node re-entrant tachycardia

Question 40

narrow complex type of rhythms

Answer 40

Atrial fibrillation
Atrial flutter with variable block
Multifocal atrial tachycardia

Question 41

inferior surface of the heart

Answer 41

II, III, and aVF: inferior surface of the heart

Question 42

anterior surface of the heart

Answer 42

V1 to V4: anterior surface

Question 43

lateral surface of the heart

Answer 43

I, aVL, V5, and V6: lateral surface

Question 44

right atrium and cavity of the left ventricle

Answer 44

V1 and aVR: right atrium and cavity of left ventricle

Question 45

characteristics of P wave

Answer 45

Positive in leads I and II
Best seen in leads II and V1
Commonly biphasic in lead V1
<3 small squares in duration
<2.5 small squares in amplitude

Question 46

diagnostic criteria for RBBB

Answer 46

QRS duration ⩾0.12 s
A secondary R wave (R’) in V1 or V2
Wide slurred S wave in leads I, V5, and V6
Associated feature
ST segment depression and T wave inversion in the right precordial leads

Question 47

diagnostic criteria for LBBB

Answer 47

QRS duration of ⩾0.12 s
Broad monophasic R wave in leads 1, V5, and V6
Absence of Q waves in leads V5 and V6
Associated features
Displacement of ST segment and T wave in an opposite direction to the dominant deflection of the QRS complex (appropriate discordance)
Poor R wave progression in the chest leads
RS complex, rather than monophasic complex, in leads V5 and V6
Left axis deviation—common but not invariable finding

Question 48

what are the fascicular blocks? [3]

Answer 48

Block of the left anterior and posterior hemifascicles gives rise to the hemiblocks. Left anterior hemiblock is characterised by a mean frontal plane axis more leftward than −30° (abnormal left axis deviation) in the absence of an inferior myocardial infarction or other cause of left axis deviation. Left posterior hemiblock is characterised by a mean frontal plane axis of >90° in the absence of other causes of right axis deviation.

Bifascicular block is the combination of right bundle branch block and left anterior or posterior hemiblock. The electrocardiogram shows right bundle branch block with left or right axis deviation. Right bundle branch block with left anterior hemiblock is the commonest type of bifascicular block. The left posterior fascicle is fairly stout and more resistant to damage, so right bundle branch block with left posterior hemiblock is rarely seen.

Trifascicular block is present when bifascicular block is associated with first degree heart block. If conduction in the dysfunctional fascicle also fails completely, complete heart block ensues.

Question 49

atrial tachycardia

Answer 49

Abnormal P wave morphology
Atrial rate 100-250 beats/min
Ventricular rhythm usually regular
Variable ventricular rate

Question 50

atrial flutter

Answer 50

Undulating saw-toothed baseline F (flutter) waves
Atrial rate 250-350 beats/min
Regular ventricular rhythm
Ventricular rate typically 150 beats/min (with 2:1 atrioventricular block)
4:1 is also common (3:1 and 1:1 block uncommon)

Question 51

atrial fibrillation

Answer 51

P waves absent; oscillating baseline f (fibrillation) waves
Atrial rate 350-600 beats/min
Irregular ventricular rhythm
Ventricular rate 100-180 beats/min

Question 52

as a general rule, what is urgently needed for some patients

Answer 52

As a general rule the faster the ventricular rate, the more likely the presence of symptoms—for example, chest pain, faintness, and breathlessness. Urgent treatment is needed for severely symptomatic patients with a narrow complex tachycardia.

Question 53

causes of torsades de pointes

Answer 53

Antiarrhythmic drugs: class Ia (disopyramide, procainamide, quinidine); class III (amiodarone, bretylium, sotalol) * Hypokalaemia
* Antibacterials: * Hypomagnesaemia
erythromycin, fluoquinolones, Congenital syndromes
trimethoprim * Jervell and Lange-Nielsen   syndrome
* Other drugs: terfenadine, cisapride, tricyclic antidepressants, haloperidol, lithium, phenothiazines, chloroquine, thioridazine * Romano-Ward syndrome
Other causes
* Ischaemic heart disease
* Myxoedema
* Bradycardia due to sick sinus   syndrome or complete heart   blocka

Question 54

what is WPW? [1]

Answer 54

In this syndrome an accessory pathway (the bundle of Kent) connects the atria directly to the ventricles. It results from a failure of complete separation of the atria and ventricles during fetal development.

Question 55

WPW on an ecg

Answer 55

It is transmitted rapidly to the ventricular myocardium, and consequently the PR interval is short. However, because the impulse enters non-specialised myocardium, ventricular depolarisation progresses slowly at first, distorting the early part of the R wave and producing the characteristic delta wave on the electrocardiogram. This slow depolarisation is then rapidly overtaken by depolarisation propagated by the normal conduction system, and the rest of the QRS complex appears relatively normal.

Question 56

danger of misdiagnosis VT

Answer 56

The safest option is to regard a broad complex tachycardia of uncertain origin as ventricular tachycardia unless good evidence suggests a supraventricular origin
If a ventricular tachycardia is wrongly treated as supraventricular tachycardia, the consequences may be extremely serious
Giving verapamil to a patient with ventricular tachycardia may result in hypotension, acceleration of the tachycardia, and deatha

Question 57

how to differentiate between VT and atrial fibrillation with aberrant conduction or pre-excitation

Answer 57

In ventricular tachycardia the rhythm is regular or almost regular; if the rhythm is obviously irregular the most likely diagnosis is atrial fibrillation with either aberrant conduction or pre-excitation

Question 58

is ECG good enough for MI

Answer 58

Electrocardiography is not sufficiently specific or sensitive to be used without a patient’s clinical history

Question 59

criteria for the size of the R wave

Answer 59

1/8 size of the R wave
<2/3 size of the R wave
Height <10 mm
Often, they are tall, inverted, flattened or biphasic

Question 60

T wave inversion

Answer 60

T wave inversion can be normal
It occurs in leads III, aVR, and V1 (and in V2, but only in association with T wave inversion in lead V1)

Question 61

When should I be concerned about T wave inversion?

Answer 61

Myocardial ischaemia may also give rise to T wave inversion, but it must be remembered that inverted T waves are normal in leads III, aVR, and V1 in association with a predominantly negative QRS complex. T waves that are deep and symmetrically inverted (arrowhead) strongly suggest myocardial ischaemia.

In some patients with partial thickness ischaemia the T waves show a biphasic pattern. This occurs particularly in the anterior chest leads and is an acute phenomenon. Biphasic T wave changes usually evolve and are often followed by symmetrical T wave inversion. These changes occur in patients with unstable or crescendo angina and strongly suggest myocardial ischaemia.

Question 62

indications for thrombolytic treatment

Answer 62

ST elevation >1 mm in two contiguous limb leads or >2 mm in two contiguous chest leads
Posterior myocardial infarction
Left bundle branch blocka

Question 63

anatomical relationship leads

Answer 63

Inferior wall—Leads II, III, and aVF
Anterior wall—Leads V1 to V4
Lateral wall—Leads I, aVL, V5, and V6

Question 64

ECG changes of someone with acute PE

Answer 64

Sinus tachycardia
Atrial flutter or fibrillation
S1, Q3, T3 pattern
Right bundle branch block (incomplete or complete)
T wave inversion in the right precordial leads
P pulmonale
Right axis deviation

Question 65

Sx of Sjogren’s

Answer 65

The two main symptoms of Sjogren’s syndrome are:

Dry eyes. Your eyes might burn, itch or feel gritty — as if there’s sand in them.
Dry mouth. Your mouth might feel like it’s full of cotton, making it difficult to swallow or speak.
Some people with Sjogren’s syndrome also have one or more of the following:

Joint pain, swelling and stiffness
Swollen salivary glands — particularly the set located behind your jaw and in front of your ears
Skin rashes or dry skin
Vaginal dryness
Persistent dry cough
Prolonged fatigue

Question 66

Cx of Sjogren’s

Answer 66

The most common complications of Sjogren’s syndrome involve your eyes and mouth.

Dental cavities. Because saliva helps protect the teeth from the bacteria that cause cavities, you’re more prone to developing cavities if your mouth is dry.
Yeast infections. People with Sjogren’s syndrome are much more likely to develop oral thrush, a yeast infection in the mouth.
Vision problems. Dry eyes can lead to light sensitivity, blurred vision and corneal damage.
Less common complications might affect:

Lungs, kidneys or liver. Inflammation can cause pneumonia, bronchitis or other problems in your lungs; lead to problems with kidney function; and cause hepatitis or cirrhosis in your liver.
Lymph nodes. A small percentage of people with Sjogren’s syndrome develop cancer of the lymph nodes (lymphoma).
Nerves. You might develop numbness, tingling and burning in your hands and feet (peripheral neuropathy).

Question 67

thromboprophylaxis after surgery [2]

Answer 67

The ACCP recommends the use of enoxaparin 30 mg subcutaneously (SC) twice daily started either 12 hours before or 12 to 24 hours after hip arthroplasty for at least 10 days and up to 35 days postoperatively

Question 68

Mx of pressure sores

Answer 68

a moist wound environment encourages ulcer healing. Hydrocolloid dressings and hydrogels may help facilitate this. The use of soap should be discouraged to avoid drying the wound
wound swabs should not be done routinely as the vast majority of pressure ulcers are colonised with bacteria. The decision to use systemic antibiotics should be taken on a clinical basis (e.g. Evidence of surrounding cellulitis)
consider referral to the tissue viability nurse
surgical debridement may be beneficial for selected wounds

Question 69

what is the waterlow score? [1]

Answer 69

The Waterlow score is widely used to screen for patients who are at risk of developing pressure areas. It includes a number of factors including body mass index, nutritional status, skin type, mobility and continence.

Question 70

What is FTD? [2]

Answer 70

Frontotemporal lobar degeneration (FTLD) is the third most common type of cortical dementia after Alzheimer’s and Lewy body dementia.

Question 71

Common features of FTD

Answer 71

Onset before 65
Insidious onset
Relatively preserved memory and visuospatial skills
Personality change and social conduct problems

Question 72

What type of drug is donepezil? [1]

Answer 72

Acetyolcholinesterase inhibitor

Question 73

type of med is meropenem? [1]

Answer 73

broad-spectrum carbapenem antibiotic

Question 74

first, second and third line Tx for dementia

Answer 74

NICE updated it’s dementia guidelines in 2018
the three acetylcholinesterase inhibitors (donepezil, galantamine and rivastigmine) as options for managing mild to moderate Alzheimer’s disease
memantine (an NMDA receptor antagonist) is in simple terms the ‘second-line’ treatment for Alzheimer’s, NICE recommend it is used in the following situation reserved for patients with
moderate Alzheimer’s who are intolerant of, or have a contraindication to, acetylcholinesterase inhibitors
as an add-on drug to acetylcholinesterase inhibitors for patients with moderate or severe Alzheimer’s
monotherapy in severe Alzheimer’s

Question 75

when is donepezil CI? [1]

Answer 75

is relatively contraindicated in patients with bradycardia
adverse effects include insomnia

Question 76

when should antipsychotic be used for dementia patients? [1]

Answer 76

NICE does not recommend antidepressants for mild to moderate depression in patients with dementia
antipsychotics should only be used for patients at risk of harming themselves or others, or when the agitation, hallucinations or delusions are causing them severe distress

Question 77

why does sundowning happen? [2]

Answer 77

Sundowning has several causes. As the day goes on, the person with dementia becomes more tired, and this can lead to their dementia symptoms worsening. Hunger, thirst and physical pain can also play a part.

As darkness falls, streetlights come on and people settle in for the evening. These changes can make the person increasingly concerned that they are in the wrong place, or that they have forgotten to do something vital during the day

Question 78

how do cholinesterase inhibitors work? [1]

Answer 78

The only role for cholinesterase inhibitors is to improve some cognitive function and improvement in activities of daily living. There is no role for cholinesterase inhibitors in advanced Alzheimer’s disease.

Question 79

macro, micro and biochemical changes in AD

Answer 79

macroscopic:
widespread cerebral atrophy, particularly involving the cortex and hippocampus
microscopic:
cortical plaques due to deposition of type A-Beta-amyloid protein and intraneuronal neurofibrillary tangles caused by abnormal aggregation of the tau protein
hyperphosphorylation of the tau protein has been linked to AD
biochemical
there is a deficit of acetylcholine from damage to an ascending forebrain projection

Question 80

Ix in dementia

Answer 80

in primary care, a blood screen is usually sent to exclude reversible causes (e.g. Hypothyroidism). NICE recommend the following tests: FBC, U&E, LFTs, calcium, glucose, ESR/CRP, TFTs, vitamin B12 and folate levels. Patients are now commonly referred on to old-age psychiatrists (sometimes working in ‘memory clinics’).
in secondary care, neuroimaging is performed* to exclude other reversible conditions (e.g. Subdural haematoma, normal pressure hydrocephalus) and help provide information on aetiology to guide prognosis and management

Question 81

What is CI in PD? [1]

Answer 81

Haloperidol is contraindicated in patients with Parkinson’s disease

Question 82

which medications can be used in LBD? [2]

Answer 82

both acetylcholinesterase inhibitors (e.g. donepezil, rivastigmine) and memantine can be used as they are in Alzheimer’s. NICE have made detailed recommendations about what drugs to use at what stages. Please see the link for more details

Question 83

Which medications should be avoided in LBD? [2]

Answer 83

neuroleptics should be avoided in Lewy body dementia as patients are extremely sensitive and may develop irreversible parkinsonism. Questions may give a history of a patient who has deteriorated following the introduction of an antipsychotic agent

Question 84

features of LBD [3]

Answer 84

progressive cognitive impairment
typically occurs before parkinsonism, but usually both features occur within a year of each other. This is in contrast to Parkinson’s disease, where the motor symptoms typically present at least one year before cognitive symptoms
cognition may be fluctuating, in contrast to other forms of dementia
in contrast to Alzheimer’s, early impairments in attention and executive function rather than just memory loss
parkinsonism
visual hallucinations (other features such as delusions and non-visual hallucinations may also be seen)

Question 85

Dx of dementia [3]

Answer 85

usually clinical
single-photon emission computed tomography (SPECT) is increasingly used. It is currently commercially known as a DaTscan. Dopaminergic iodine-123-radiolabelled 2-carbomethoxy-3-(4-iodophenyl)-N-(3-fluoropropyl) nortropane (123-I FP-CIT) is used as the radioisotope. The sensitivity of SPECT in diagnosing Lewy body dementia is around 90% with a specificity of 100%

Question 86

features of normal pressure hydrocephalus [3]

Answer 86

memory impairment, urinary frequency, and balance problems/gait deviations

Question 87

Tx of NPH [2]

Answer 87

The treatment is surgical placement of a ventriculoperitoneal shunt to drain excess CSF into the lining of the abdomen where the CSF will eventually be absorbed. NPH is often misdiagnosed as other conditions including Meniere’s disease due to balance problems, Parkinson’s disease (due to gait) or Alzheimer’s disease (due to cognitive dysfunction).

Question 88

gait in NPH

Answer 88

The gait abnormalities in NPH may bear resemblance to a gait associated with Parkinson’s disease.

Question 89

how common are dementia and urinary incontinence in NPH? [2]

Answer 89

Dementia presents as progressive cognitive impairment which is present in 60% of patients at time of treatment. This is caused by distortions predominantly at the frontal lobe and the subcortex.[6] Initial deficits involve planning, organization, attention, and concentration. Further deficits include difficulty managing finances, taking medications, driving, keeping track of appointments, daytime sleeping, short-term memory impairments, and psychomotor slowing. Late stage features include apathy, reduced drive, slowed thinking, and reduced speech.

Urinary incontinence appears late in the illness, and is present in 50% of patients at time of treatment. Urinary dysfunction begins as increased frequency often at night, and progresses to urge incontinence and permanent incontinence.[6]

Question 90

Dx of NPH [2]

Answer 90

Gradual onset after age 40 years, symptoms duration of ≥ 3–6 months, clinical evidence of gait or balance impairment, and impairment of cognition or urinary incontinence
Imaging from magnetic resonance imaging (MRI) or computed tomography (CT) is needed to demonstrate enlarged ventricles and no macroscopic obstruction to cerebrospinal fluid flow. Imaging should show an enlargement to at least one of the temporal horns of lateral ventricles, and impingement against the falx cerebri resulting in a callosal angle ≤ 90° on the coronal view, showing evidence of altered brain water content, or normal active flow (which is referred to as “flow void”) at the cerebral aqueduct and fourth ventricle.

Question 91

Tx for NPH? [3]

Answer 91

Ventriculoperitoneal shunts
For suspected cases of NPH, CSF shunting is the first-line treatment. The most common type used to treat NPH is ventriculoperitoneal (VP) shunts, which drain CSF fluid to the peritoneal cavity. Adjustable valves allow fine-tuning of CSF drainage. NPH symptoms reportedly improve in 70–90% of patients with CSF shunt. Risk-benefit analyses have shown beyond any doubt that surgery for NPH is far better than conservative treatment or the natural course.[9]

Gait symptoms improve in ≥ 85% patients. Cognitive symptoms improve in up to 80% of patients when surgery is performed early in the disease course. Urgency and incontinence improves in up to 80% of patients, but only in ≤ 50–60% of patients with shunt implanted late in disease course. The most likely patients to show improvement are those who show only gait deviation, mild or no incontinence, and mild dementia. The risk of adverse events related to shunt placement is 11%, including shunt failure, infections such as ventriculitis, shunt obstruction, over- or under-drainage, and development of a subdural hematoma.[13][14][15]

Medications
No medications are effective for primary NPH. Acetazolamide and other diuretics are not recommended except for limited use in patients who are not candidates for placement of a shunt.[citation needed]

Question 92

adverse effect of donepezil [2]

Answer 92

adverse effects of donepezil include insomnia

Question 93

severity of dementia

Answer 93

normal: 30- 27
Mild: 26- 22
Mod.: 21-10
Severe: 9-0

Question 94

when to Rx dementia medications? [2]

Answer 94

in mild ot moderate AD

Question 95

memantine mild dementia

Answer 95

NICE guidelines do not support the use of memantine in mild dementia

Question 96

amtriptylline in dementia

Answer 96

One example of this is the use of tricyclic antidepressants in patients with dementia, due to the risk of worsening cognitive impairment.

Question 97

Mx for RLS

Answer 97

pramipexole

Question 98

presentation of VD

Answer 98

Several months or several years of a history of a sudden or stepwise deterioration of cognitive function.

Question 99

epidemiology of VD [2]

Answer 99

VD is thought to account for around 17% of dementia in the UK
Prevalence of dementia following a first stroke varies depending on location and size of the infarct, definition of dementia, interval after stroke and age among other variables. Overall, stroke doubles the risk of developing dementia.
Incidence increases with age

Question 100

which type of dementia often has FH? [1]

Answer 100

FTD