M and E and NCD's Flashcards

1
Q
  • What is the difference between `Monitoring and Evaluation’
A

Monitoring is the routine daily assessment of ongoing activities - what has been DONE. Evaluation is the EPISODIC assessment of overall achievement - what is the IMPACT of the activity.

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2
Q
  • What components of interventions are monitored and evaluated?
A
  • Inputs: people, training, equipmment and resources put into a project to achieve outputs.
  • Outputs: activities or services delivered, eg HIV/AIDS prevenction, care and support services.
  • Outcomes: Changes in behaviour or skills, esp safer HIV prevention practices and increased ability to cope with AIDS.
  • Impacts: major measrable health impacts, esp reduced transmission rates of stds and reduced AIDS impacts.
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3
Q

INCREMENTAL COST-EFFECTIVENESS

A

Incremental cost-effectiveness ratio:= Difference in cost / Difference in health years= Cost / HLY

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4
Q
  • WORLD HEALTH REPORT“REDUCING RISKS, PROMOTING HEALTHY LIFE: Substantial health gains for relatively modest expenditures.
  • Provide some examples.
A
  • substantial health gains for relatively modest expenditures: Combinations of personal and non-personal (population) interventions are cost-effective.
    • For children, Vitamin A and Zinc provision together with treatment of pneumonia and diarrhoea
    • For unsafe sex: preventive interventions plus some ARV
    • For CVDs: population salt reduction and mass media with treatment;
    • Addictions: taxation, comprehensive bans on advertising
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5
Q

What is vertical equity?

A

Aristotle’s formal theory of distributive justice makes the distinction between vertical and horizontal equity: horizontal equity refers to equity between people with the same health care needs, whilst vertical equity refers to those with unequal needs should receive different or unequal health care. i) Vertical equity - is the unequal treatment of unequals and can be justified on the basis of morally relevant factors; however morally irrelevant factors should not be the basis for employing vertical equity. Morally relevant factors: Need, Ability to benefit, Autonomy, Deservingness. Morally irrelevant factors: Age & Sex, Ethnicity, Income, class

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6
Q

What is demographic transition

A

A trend of reducing Crude Birth Rate and a reducing Crude Death Rate.

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7
Q

What are the 4 stages of Demographic Transition

A
  1. Deaths and Births are high 2. Deaths begin to reduce but medicine and PH is not advanced. CBR remains high because agrarian societies with high labour needs. 3. Deaths reduce. CBR starts to decline due to more women’s participatin in society and reduced need for families to have many children. 4. CBR is sustained at a really low level with some countries below replacement medicine.
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8
Q

Population Pyramids: What do they look like in stages of Demographic transition?

A
  1. Declining: Broad based, marked mortality. 2. Expanding: More compressed, because of falling brirth rate 3. Stationery: Looks more like half ellipse. Minimal Childhood death rated, straight edges with fall off only at advanced age. 4. Egg shaped because Birth rates at bottom have fallen off.
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9
Q

Life Expectancy, what is it and what is the main driver.

A

LE used to estimate expected number of years of life remaining at any given age. In countries with high infant mortality rated, the life expectancy at birth is highly sensitive to the rate of death in the first few years of life.

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10
Q

What is endomyocardial fibrosis?

A
  • Endomyocardial fibrosis is a form of endemic restrictive cardiomyopathy that affects mainly children and adolescents, and is geographically restricted to some poor areas of Africa, Latin America and Asia. It is a condition with high morbidity and mortality, for which no effective therapy is available. Although several hypotheses have been proposed as triggers or causal factors for the disease, none are able to explain the occurrence of the disease worldwide.
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11
Q

What are the BCSH recommendations wrt prophylactic antibiotics in splenectomized patients?

A

The available data supports the continued use of penicillin prophylaxis (or equivalent) in hyposplenic patients up to aged 16 years and those over 50 years. Patients who have inadequate responses to pneumococcal vaccination or who have had a previous episode of invasive pneumococcal disease remain at high risk and should continue prophylaxis indefinitely. After splenectomy for trauma the risk is greatest in the immediate post-operative period, and antibiotic prophylaxis should include this period at least (Malangoni et al, 1984).

Recommendations

Life long prophylactic antibiotics should be offered to patients considered at continued high risk of pneumo- coccal infection (B, C).

  • Factors associated with high risk of invasive pneumococ- cal disease in hyposplenism include: aged less than 16 years or greater than 50 years, inadequate serological response to pneumococcal vaccination, a history of previous invasive pneumococcal disease, and splenectomy for underlying haematological malignancy particularly in the context of on-going immunosuppression (B, C).
  • Patients not at high risk should be counselled regarding the risks and benefits of lifelong antibiotics and may choose to continue or discontinue prophylaxis (C).
  • All patients should carry a supply of appropriate antibi- otics for emergency use (C).
  • Patients developing symptoms and/or signs of infection, despite the above measures, must be given systemic antibiotics and admitted urgently to hospital (B, C).
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12
Q

What does the incidence of Type 1 diabetes in the tropics compare with Europe.

A
  • it is much lower eg. 2/100,000 Tanzania c/w 18.5/100,000 in UK
  • Theories
    • Sunshine hypothesis (vit D)
    • Hygeine hypothesis (viral infections, overcrowding)
    • Cow’s mile hypothesis (delayed introduction)
    • Accelerator hypothesis (body wt)
    • Different viral ecologies? (mine)
    • Don’t know
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13
Q

What is the accelerator hypothesis wrt the pathogenesis of diabetes?

A
  • The accelerator hypothesis argues that type-1 and type-2 diabetes are the same disorder of insulin resistance set against different genetic backgrounds. It identifies three processes which variably accelerate beta cell loss: constitution, insulin resistance and the immune response to it. None of the accelerators leads to diabetes in the absence of weight gain, a trend which the hypothesis deems central to the rising incidence of all diabetes in the industrially developed and developing world. Weight gain causes an increase in insulin resistance, which results in the weakening of glucose control. The rising blood glucose accelerates beta cell apoptosis (glucotoxicity) and, by increasing beta cell immunogenicity, further accelerates apoptosis in a subset genetically predisposed to an intense immune response. Rather than overlap between the two types of diabetes, the accelerator hypothesis envisages overlay–one a subset of the other. Body mass is central to the development and rising incidence of all diabetes. Only tempo distinguishes type 1 from type 2. The control of weight gain, and with it insulin resistance, could be the means of preventing both by slowing their progression
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14
Q

Identify the so-called varieties of tropical diabetes, the 3 types with unusual presentation.

A
  • MRDM (“Malnutrition-related diabetes mellitus”)
  • Atypical ketosis-prone type 2 dm
  • Anti-retroviral drug-induced type 2 DM
    • some evidence of a rise in incidence following start of ARV
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15
Q

How does the natural hx of diabetes differ in the tropics?

A
  • High mortality: maybe only 30-40% survival at 5 yrs post dx
  • due to
    • insulin tx and availability
    • metabolic and infective complications
    • later mortality includes renal and vasc disease
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16
Q

What is the relationship of Diabetes and TB in LMIC?

A
  • diabetes pts have 2-3 times risk of TB
  • 15-20% of TB pts may have T2DM
  • suggest bidirectional screening (TB for DM and DM for TB)
  • diabetes may remit after TB tx.
17
Q

Assessing diabetes control

“Where there is no HgbA1C.”

A
  • wt, osmotic sx and hypo frequency as monitored endpoints for tx
  • in type 2 DM, nocturia (>1) predicts FBG>8.0 mmol
  • RBG >13 predicts HbA1c > 8.5%
18
Q

Treatment of Epilepsy

Describe a practical, low cost 1st line approach.

A
  • Phenobarbitol monotherapy
  • highly effective, simple, low side effects
  • start with 30 mg od, f/u at monthly intervals with log of seizure frequency, set targe and expectations, titrate up to 90 mg (30, 60, 90)
19
Q

What are the risks of teratogenicity with commonly used anti-seizure meds and how would this inluence your choice in pregnancy?

A
  • valproate major problem, 9.3% risk of major malformations, 30%-40% have later developmental and cognitive impairment
  • other drugs less but sig malformation risks. (Other outcome risks are low)
    • phenobarb 5.5%
    • carbamazepine 2.9%
    • lamotrigine 2.0%
  • therefore avoid valproate in women likely to become pregant, assess risks with others on case by case basis
  • if possible give folic acid 5 mg daily to women on seizure meds who might get pregnant
20
Q

Anticonvulsants and ARV’s

A
  • many induce cytochrome P450
  • esp phenytoin, phenobarb and CBZ
  • others rarely available
  • take individual approach monitor ARV responses closely use interactions tool
21
Q

What are some etiological theories/factors that attempt to account for rising incidence of hypertension in Africa?

A
  • •Environmental – salt, obesity, alcohol
  • •Genetic – reduced salt excretion capacity eg Afro-Carribeans (“Slave Hypothesis”)
  • •Low birth weight (“Foetal Origins Hypothesis”)
  • •Urbanisation and epidemiological transition
  • •ARVs – “metabolic syndrome”
  • Lifestyle factors
    • nb marked increase in HT prevalence with rural-urban migration, occurs early before wt gain
    • poss due to less exercise, more insuline resistance
    • NaCl and Etoh
22
Q

Stroke Mortality and Hypertension

A
  • mostly infarcts rather than hemorrhage
  • high case fatility rate (45% in first wk)
23
Q

Management of Hypertensive Crisis

How, given limited availability of drugs>

A
  • consider methyldopa 1 gm stat and 500 mg 4 hrly
  • hydralazine 10 mg im q 3-4 hrs
24
Q

What are the 5 commonest causes of NCD in Tanzania

A
  • Trauma
  • Heart Failure
  • Stroke
  • Cancer
  • Diabetes