Diseases and others... Flashcards

1
Q

In what conditions should amyloidosis be considered as a differential?

A

Nephrotic syndrome
Cardiomyopathies
Peripheral neuropathies

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2
Q

What are the effective management strategies in allergy?

A

Avoidance of the allergen
Antihistamine - H1 receptor antagonist - Cetirizine
Corticosteroids - hydrocortisone/prednisolone
Omalizumab = monoclonal antibody vs. IgE
Adrenaline = for anaphylactic shock

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3
Q

What are the most common allergens?

A

Insect stings
Latex
Food allergies
Drugs

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4
Q

What is the most common cause of non IgE mediated mast cell degranulation?

A

Drug allergy

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5
Q

What are the clinical manifestations of anaphylaxis?

A
Tachycardia
Hypotension
Urticaria
Wheeze and broncho-constriction
Stridor
Flushing and sweating
Itching on palms of hands and soles of feet
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6
Q

What is the difference between non pitting and pitting oedema?

A

Pitting oedema occurs in organ failure (heart, liver kidney) when the plasma oncotic pressure is too low to draw water back into the blood vessels by osmosis = transudate.

Non-pitting oedema is mainly caused by lymphoedema/angioedema when the interstitium fills with solutes and attracts water out into the interstitium = exudate.

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7
Q

What are the different classifications of transplant rejection and their treatments?

A

Hyperacute rejection = 30 days = minimise drug toxicity and control hypertension.

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8
Q

What is the MOA of the main anti-rejection drugs.

A

Anti-proliferative agents:
Azathioprine = inhibits lymphocyte proliferation by blocking DNA synthesis

Calcineurin inhibitors:
Cyclospoirn/Tacrolimus = Blocks T-cell signalling to prevent lymphocyte proliferation and block cytokine transcription. Calcineurin up regulates Il2 = T-cell proliferation.

Corticosteriods:
Betamethazone/prednisolone = decreases inflammatory and immune related proteins by down-regulating gene transcription

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9
Q

What is the mechanism of increasing T-cell and Ig affinity during an infection?

A

Somatic (VDJ) recombination

The VDJ genes are all part of the variable region of the future antibody. There is also a constant gene which codes for the constant regions of the antibody.

Recombination = removing the introns between the V, D and J segments, bringing them closer together with removal of unwanted segments of each (VDJ) to change the final variable site of the Ig to increase affinity.

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10
Q

What are the protective mechanisms of the body in a hot and cold environment?

A

COLD:
Shivering
Peripheral vasoconstriction
Behavioural changes

HOT:
Peripheral vasodilation
Behavioural changes
Decreased muscle activity and lethargy
Sweating to increase evaporative heat loss
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11
Q

What is hypothermia?
Who is at risk?
What are the main clinical features?

A

When the body is unable to maintain a core temperature above 35˚C due to extreme cold.

Extremities of age are most at risk. Babies = high surface area to volume ration. Elderly = co-morbidities and reduced protective measures.

Mild hypothermia = confusion, cold extremities, dehydration, shivering.

Severe hypothermia = reduced consciousness, stiffness, failed vasoconstriction, bradycardia, hypotension

Can progress to coma and death but resuscitative measures should be undertaken until ‘warm and dead’ as severe cold can prolong a near-death state.

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12
Q

What are the common heat illnesses ranging from least to most severe?

A

Heat cramp = vigorous exercise and profuse sweating in hot weather with no rise in core temperature. Made worse by replacing water but not salts.

Heat syncope = Faint caused by severe peripheral vasodilation and drop in peripheral resistance in hot weather.

Heat exhaustion = Inadequate salt and water replacement with raise in body temperature 40˚C. Failure of thermoregulatory systems and can lead to death. heat exhaustion + (N+V, confusion, muscle tremor, aggression, loss of conscousness). Treated with fluid replacement and rapid cooling.

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13
Q

Describe the basic hormonal mechanisms for the control of hunger.

A

Hunger:
Stomach –> ghrelin –> hypothalamus –> neuropeptide Y –> hunger

Satiety:
Pancreas –> insulin
Intestines –> GLP-1, peptide YY, polypeptides
Adipose tissue –> leptin
–> hypothalamus –> decrease NPY –> satiety

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14
Q

What are the complications of diabetes?

A
Coronary heart disease
Stroke
Diabetes
Hypertension
Non-alcoholic steatohepatitis
Cirrhosis
Exertional dyspnoea
Sleep apnoea
Respiratory failure
Osteoarthritis
Varicose veins
Breast and uterus cancer
Polycystic ovary syndrome
Gall stones
Colorectal cancer
Skin infections
Psychological problems
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15
Q

What is metabolic syndrome?

A

Type 2 diabetes
Hypertension
Hyperlipidaemia
Obesity

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16
Q

What are some of the reasons for the increasing prevalence of obesity?

A
Increased portion sizes
Snacking, loss of regular meals
Increase in energy dense food
Increased affluence
Increased use of cars
Less walking
More automation and less manual labour
Less sports in schools
Computing increase
Increased central heating?
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17
Q

What are some of the potentially reversible causes of weight gain?

A

Hypothyroidism
Cushing’s
Insulinoma
Hypothalamic tumours

Drugs -
Tricyclic antidepressants
Sulphonylureas
Contraceptive pill (oestrogen containing)
Corticosteroids
Sodium valproate
Beta blockers
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18
Q

What management is available for obesity and what are the BMI cut offs?

A

Surgery = 40 w/o co-morbidity, 35 with

Drugs (orlistat, sibutramine) = 30 w/o cormorbidity, 27 with.

Below this = low calorie diet and improve eating behaviour, exercise and treat risk factors for disease.

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19
Q

What are the two main drugs used for weight loss?

A

Orlistat = pancreatic lipase inhibitor causing non-absorption of fats and excretion = severe steatorrhea = behaviour modifying drug.

Sibutramine = 5HT3 receptor agonist to decrease appetite for food. Nor-adrenergic side effects make this drug less desirable in obese patients so is 2nd line to orlistat.

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20
Q

What are the main forms of bariatric surgery?

A

Banded gastroplasty to permanently decrease stomach size.

Gastric banding to reversibly control stomach size and restrict intake.

Rue en Y gastric bypass to maintain passageway for pancreatic enzymes.

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21
Q

What is the main consequence of vitamin A deficiency?

A

Blindness - mainly in children in the developing world

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22
Q

What are the consequences of vitamin D deficiency?

A

Rickets in children

Osteomalacia in adults

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23
Q

What are the consequences of vitamin K deficiency?

A

Delayed coagulation and bleeding

24
Q

What are the consequences of thiamine (vit. B1) deficiency?

A

Beri-Beri (usually seen in chronic alcoholics due to poor diet and reduced liver storage)

  • Peripheral neuropathy (w/ wrist and fot drop)
  • Korsakoff’s psychosis
  • Wernicke’s encephalopathy
  • Pulmonary and peripheral oedema
25
Q

What are the consequences of vitamin B12 and folate deficiency?

A

Macrocytic megaloblastic anaemia
In pregnancy = spina bifida

Subacute combined degeneration of the spinal cord = demyelination of the posterior and lateral spinal tracts (B12 deficiency.)

B12 deficiency must be treated before the folate to avoid precipitating this disease. If folate is given first it will cause methlyation of the B12 so it can’t precipitate in the formation of myelin sheath.

26
Q

What are the consequences of vitamin C deficiency?

A

Scurvy

Defective collagen formation and wound healing. With defective platelets (contain lots of Vit. C)

Swollen, bleeding gums
Skin haemorrhage and bruising
GI bleeding
Anaemia
Poor wound healing
27
Q
What are the main commensal organisms of the:
Oral cavity
Skin
Vagina
Pharynx
Small bowel
Large bowel
A

Oral cavity (Strep. viridans, candida)

Skin (Staph. aureus, corynebacterium, Staph. epidermidis)

Vagina (lactobacillus, Staph. aureus, candida, enterobacteriacea)

Pharynx (H. influenzae, M. catarrhalis, N. meningitidis, Staph. aureus, Strep. pneumonia, Strep. pyogenes)

Small bowel = fairly low bacterial count. Distally increasing (candida)

Large bowel (Enterobacteriaceae)

28
Q

What are the mechanisms of antimicrobial resistance?

A
Efflux of the drug from the cell 
Impermeability of the membrane 
Enzyme to inactivate then drug
Change of metabolic pathway 
Over expression of  active site
29
Q

What organisms are penicillins effective against?

A

Gram +ve organisms (- staphylococci)

Anaerobic organisms

30
Q

What organisms are cephlasporins effective against?

A

Mainly gram +ve but later generations have improved cover over gram -ve organisms

31
Q

What organisms are carbapenems effective against?

A

The most broad spectrum of the B-lactam antibiotics.
Include activity against anaerobes as well as gram +ve

Used rarely as a last line in severely resistant organisms.

32
Q

What organisms are amino glycosides effective against?

A

Gram -ve organisms

Act synergistically with B-lactams as they are generally effective against opposite organism types.

33
Q

What organisms are quinolone antibiotics effective against?

A

Gram -ve

34
Q

What organisms are glycopeptide antibiotics effective against?

A

Purely gram +ve

Used for resistant organisms (MRSA, C.diff)

35
Q

What organisms is metronidazole effective against?

A

Strict anaerobes
C. diff
Some protozoa (Giardia)

36
Q

What are the aspects of a patient that should be assessed in a general mental history?

A

General appearance (clothing, neglect)
Speech (slow, pressured)
Mood (facial expression, posture, movement)
Thoughts (guilt, depression, anxiety)
Beliefs
Perception (illusions and hallucinations)
Cognitive impairment

37
Q

What are the categories within cognitive function?

A

Memory
Intelligence
Concentration
Orientation (person, time and place)

38
Q

What are the symptoms of anxiety illness?

A

Psychological: Apprehension, irritability, worry, fear, lack of concentration

Somatic: sweating, tachycardia, palpitations, tremor, fatigue, chest pain, insomnia, headache

39
Q

What are the symptoms of depressive illness?

A

Psychological: Depressed mood, apprehension, worry, guilt, loss of interest, pessimism, loss of enjoyment

Somatic: Insomnia, fatigue, reduced weight, loss of libido, motor retardation

40
Q

What are the main stress disorders?

A

Acute stress reaction
Adjustment disorder
PTSD

41
Q

What is adjustment disorder?

A

A prolonged emotional reaction occurring within 1 month of traumatic event.
(Loss of loved one, medical diagnosis)

Depression, anxiety, anger, alcohol use, insomnia,

Pathological grief

42
Q

What is PTSD?

A

Post traumatic stress disorder
“A protracted stress response to a severe and devastating life event”
Possible delay of days-months

Insomnia, flashbacks, nightmares, sympathetic symptoms, fatigue, anxiety, depression, substance misuse, emotional blunting

Routine counselling has been shown to be ineffective for all members after a traumatic incidence. For people experiencing PTSD, counselling is useful and most symptoms disappear within 2 years.

43
Q

What are the main anxiety disorders?

A

Phobic anxiety disorder
Panic disorder
Generalised anxiety disorder
OCD

44
Q

What is the difference between phobic anxiety disorder and panic disorder?

A

Phobic anxiety = severe anxiety when presented with a specific event or circumstance. E.g. agoraphobia

Panic disorder = repeated panic attacks not associated with any specific event. (tachycardia, tachypnea, sweating, chest pain, parasthesia). Patients fear they are experiencing a serious illness (cardiac arrest)

45
Q

What is the treatment for anxiety disorders?

A

Counselling and fear management (CBT)

Antidepressants (benzodiazepines B-blockers)

46
Q

What is OCD

A

Obsessive compulsive disorder
Characterised by chronic obsessive thoughts which are unwanted and anxiety provoking and by compulsions to perform specific tasks - these relieve the feelings of anxiety
(bad things will happen if the tasks are not performed)

47
Q

What are the different mood disorders?

A

Monopolar depression (one or more episodes of low mood)

Bipolar depression (episodes of elevated mood with periods of elevated mood (manic depression))

Dysthymia (chronic, unrelenting low-grade depressed mood)

48
Q

What is the incidence of depression in the general population?

A

~5%

49
Q

What are the risk factors for depression?

A

Adverse life events
Emotional deprivation early in life
Abuse
(Chronic) medical illness

Hypo-function of 5-HT3 in the brain
Raised HPA axis = lack of -ve feedback

50
Q

What is the treatment for depression?

A

Antidepressant drugs

SSRIs (fluoxitine)
Tricyclic antidepressants (amitriptyline)
MAOI’s (phenelzine)
NARI and SSRI (venlafaxine)

51
Q

What are the two forms of bipolar disorder?

A

Type 1 = One or more manic episodes - usually at least one depressive episode

Type 2 = Regular periods of depressive episodes that are more severe than manic. At least 1 manic episode.

52
Q

Describe the aetiology of bipolar disorder.

A

Lifetime risk = 1%
Extremely heritable (80%)
Onset usually in teens
1:1 men:women

53
Q

What is schizophrenia?

A
A psychological illness characterised by:
Delusions
Hallucinations
Illusions 
Lack of insight / distorted thinking
54
Q

What are the significant interview signs of chronic alcohol misuse?

A
C = cut down?
A = anger at people commenting on drinking?
G = guilt about drinking?
E = eye opener?
55
Q

What are the side effects of chemotherapy?

Long and short term?

A
Alopecia
Mucositis
Cardiac arrhythmia
Nausea and vomiting
Diarrhoea
Acute kidney injury
Neuropathies (motor and sensory)
Neutropenia, thrombocytopenia, anaemia

Heart failure
Lung fibrosis
Amenorrhea

56
Q

What are the side effects of radiotherapy?

Long and short term?

A
Alopecia
Mucositis
Cough
Nausea and vomiting
Diarrhoea
Neutropenia

Fibrosis
Strictures
Increased risk of malignancy generally
Reduced growth (in children)

57
Q

What is the differential for acute diarrhoea?

A
Gastroenteritis (bacterial, viral, parasitic)
C. diff
Acute diverticulitis
Sepsis
Inflammatory bowel disease
Irritable bowel syndrome
Medications