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Clinical Conditions Flashcards

0
Q

Describe sickle cell anaemia:

What kind of genetic inheritance
What is replaced
Comsequence

A

Autosomal recessive
A->T = glutamate (hydrophilic) -> valine (hydrophobic)
In beta subunits of Hb

Can have trait: mainly no SCA symptoms, but protects against malaria

Creates sticky hydrophobic pocket.
Polymerised Hb causes cell to adopt sickle shape
Can block micro vasculature & cause sickle cell crisis

Crisis precipitated by factors that reduce O2 availability/promote T state (smoking, obesity, cold, infection)

Haemolytic anaemia: result of spleen removing sickled RBCs

Jaundice: excess bilirubin from excess breakdown

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1
Q

Describe amyloidosis

A

Mis folding of proteins
= insoluble form of normally soluble protein
Effects vary dependent on location
In brain = Alzheimer’s

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2
Q 
Describe cystic fibrosis:
Genetic basis
What is affected
Consequences
Treatment
A

Autosomal recessive: mutated chromosome 7. Normally 1 codon del.

Defective cystic fibrosis transmembrane regulator (CFTR) gene.

Impaired ability to transport Na+/Cl-:
Cl- doesn’t move from inside to outside cell
Na+ doesn’t follow
No solute produced outside cell / NaCl inside cell
Water doesn’t follow to dissolve solute
Mucus mot hydrated

Resp tract: ciliary escalator impaired, bacteria aren’t cleared = infection
Pancreatic duct: mucus blocks = pancreatitis, stops fat digestioon
Sweat: salty
Males: vas deferens doesn’t form = infertility

Prophalaxis for lung infections
Lipase tablets to digest fats
Recover sperm from testes; bypass vas deferens

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3
Q

Thalassaemias: 2 types

A

Alpha: decreased/absent alpha chains in Hb. Symptoms before birth
Beta chains Can form stable tetramers.

Beta: decreased/absent beta chains in Hb. Symptoms after birth:
Fetal Hb is alpha & gamma chains.
Cannot form stable tetramers
Reduced Hb = reduced O2 capacity. Anaemic symptoms

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4
Q

Haemophilia A:
Type of genetic condition
Consequences
Treatment

A

Recessive X linked

No/reduced factor VIII production: blood cant clot as well (factor Xa down by 50%)

Treat with recombinant factor VIII
Avoid thrombolytics/blood thinners

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5
Q

Scurvy:
What kind of deficiency
Consequences

A

Vit C deficiency

= Lack of prolyl hydroxylation in collagen synthesis
interchain H bind formation impaired
Unable to form stable triple helix
Collagen fibrils cant be cross linked
Reduced tensile strength
Bruising
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6
Q

Down’s Syndrome

Type of genetic condition/cause

Consequences

Diagnosis

A

Extra 21st chromosome: trisomy 21
meiotic division error or Robertsonian translocation

Characteristic facial features, impaired intelligence, heart defects, increase prevalence leukaemia, early onset Alzheimer’s

Can be screened during pregnancy

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7
Q

Edwards syndrome
Type of genetic condition
Consequences

A

Trisomy 18
‘Rocker bottom’ feet, overlapping fingers, small jaw
Live 1-2 weeks

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8
Q

Patau’s syndrome
Type of genetic condition
Consequences

A

Trisomy 13
Congenital heart defects, cleft lip etc
Median survival 2.5 days

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9
Q

Turner’s syndrome
Type of genetic condition
Consequences

A

Monosomy X
Only occurs in women
Missing one copy of small autosomal region at start of sex chromosomes
Short stature, heart defects, mild LDs, neck webbing, incertility

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10
Q

Kleinfelter’s syndrome
Type of genetic condition
Consequence

A

XXY
occurs in men
Extra chromosome = smaller testes/reduced testosterone production/lack male sex characteristics/infertility
Treat with testosterone

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11
Q

Ectopic pregnancy

A

Implantation of embryo in fallopian tube
= rupture of tube
Miscarriage, haemorrhage

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12
Q

Placenta praevia

A

Implantation of embryo in lower segment of uterine wall
Placenta blocks cervix
C section required

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13
Q

Marfan’s syndrome
Type of genetic condition
Consequences

A

Autosomal dominant
Misfolding of fibrillin
More elastic connective tissue
Tall, long digits, aortic rupture likely (arteries too elastic)

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14
Q

Ethlers-Danlos disease

A

Type 3 collagen deficiency
Loss of structure (reticulin = scaffold)
Stretchy skin, unstable joints, easy bruising etc

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15
Q

Vitiligo

A

Autoimmune destruction of melanocytes
Depigmentation
Psychosocial probs for dark skinned people

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16
Q

Alopecia areata/universalis

A

Autoimmune destruction of hair follicles

Worsened by stress

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17
Q

Psoriasis

A 
Extreme over production of skin cells
Too much corneum
Scaling
Genetic link but cause unknown
Treat with steroids
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18
Q

Malignant melanoma

A

UV damage indices mutations that = malignant cancer
Prognosis good if not penetrated basement membrane
Uncommon with darker skin: melanin provides protection

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19
Q

Oesteogenesis imperfecta
Type of genetic condition
Consequences

A

Autosomal dominant
Type 1 collagen deformity/deficiency
Major component in ground substance of bone
Severe = conversion fetal hyaline cartilage skeleton: lethal
Repeated fractured = bowed long bones
Blue sclera ? Thinning cornea due to collagen probs

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20
Q

Rickets/osteomalacia

A

Deficiency in Vit D
Less absorption of Ca2+ by small bowel
Less rigid bones
More common in darker skin: less synthesis of Vit D

Rickets: children
Bowed bones (still growing)

Oestemalacia: adults
Bone/back ache
Can be secondary to impaired hepatic/renal function (less absorption)

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21
Q

Osteoporosis

2 types

A

Both osteoclast > osteoblast

Type 1: menopausal
Oestrogen no longer mediating osteoclast function.
Fractures more likely

Type 2: old age
Loss of osteoblast function: no remodelling

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22
Q

Acromegaly

A

Too much GH
Adults:
increased bone width from intramembranous growth (periosteal)
Epiphyseal plates fuse at end of puberty so no lengthening

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23
Q

Gigantism

A

Too much GH
children:
Increased height: excessive growth from epiphyseal growth plates

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24
Q

Cretinism

A

Neonatal hypothyroidism
Retardation, short stature
Give thyroxine before 3 weeks

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25
Q

Achondroplasia
Type of genetic condition
Consequences

A

Autosomal dominant
Deformed fibroblast growth factor receptor
Decreased endochondral ossification
Short limbs, enlarged forehead, normal trunk

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26
Q

Myasthenia Gravis

A

Autoimmune destruction end plate nicotinic ACh receptors
Antibodies target nAChr on post synaptic membrane of skeletal musc
Contraction ends suddenly when [ACh] drops
End plate potentials reduced in amplitude = musc weakness/fatigue
Droopy eyelids (small musc worst affected), fatigue (esp after exercise), sudden collapse
Each quantum of Ach released produces smaller response than in more musc; less nAch receptors available (same amt of Ach released)

Treat by immunosuppressin & ACh esterase inhibitors (keep more ACh in symapse)

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27
Q

Muscular Dystrophy
Type of genetic condition
Consequences

A 
Absence (Duchenne's) or truncation (Becker's) of dystrophin
Muscle fibres tear in contraction
Ca2+ induced necrosis 
Fat & CT laid down (pseudohypertrophy)
Gower's sign (brace thighs with arms)
Degenerative
Chest musc destroyed = death
28
Q

Botulism

A

Botulism toxin blocks ACh release

No musc contraction

29
Q

Thyrotoxicosis

A

Increased BMR
protein catabolism
Atrophy

30
Q

Hypoparathyroidism

A

Lack PTH
Lack Ca 2+ absorption
Tetany

31
Q

Malignant hyperthermia
Type of genetic condition
Consequences
Treatment

A

Autosomal dominant
Life threatening reaction to general anaesthesia (succinylcholine)
Leads to release of all Ca 2+ from all sarcoplasmic reticulum
Spike in Ox Phor in skeletal musc
Temperature spike
Overwhelms control mechanism = death

Manage symptoms (paracetamol & other antipyrexials)
Dentrolene (prevents Ca 2+ release)
32
Q

Multiple sclerosis

A

Autoimmune destruction of myelin sheath & schwann cells
Decrease in conduction
Loss of function

Beta interferon
Steroids
(Mediate immune function)

33
Q

Von Gierke’s Disease
Cause
What area of the body it affects
Consequences

A

Deficiency of glucose 6 phosphatase (gluconeogeneic: hydrolysis of G6P to release free glucose)

Mainly liver & kidneys

Increased conc G6P in liver & kidneys = increased amt of normal glycogen stored
Liver & kidneys unable to release glucose btw meals to regulate BG in response to glucagon = fasting hypoglycaemia
Hepatomegaly
Failure to thrive
Ketosis: body tries to use other fuels

34
Q

Hyperthyroidism (Grave’s):

Cause (cause Grave’s)
Symptoms
Treatment

A

Increased production/release T3/T4
Graves = Autoimmune disease: produces antibodies that stimulate TSH receptors

Increased T4/T3
Decreased TSH (negative feedback)
Heat intolerance, increased BMR
Weight loss
Hyperactivity
Tachycardia
Myopathy
Goitres

Carbimazole
Radioactive iodine
Thyroidectomy

35
Q

Hypothyroidism (Hashimoto’s)

Causes (cause Hashimoto’s)
Symptoms
Treatment

A

Destruction thyroid follicles, iodine deficiency (rare)
Hashimoto’s: antibody production blocking TSH receptors

Cold intolerance, reduced BMR
Weight gain
Tiredness, lethargy
Bradycardia
Goitre
Cretinism (in children if untreated)
Skin dry/flaky

Oral thyroxine (T4)

36
Q

Galactosaemia:

Definition
Deficient enzymes (which is more common, which is rarer)
Consequences
Treatment

A

Inability to use galactose = increased levels in blood

Galactokinase (non-classical galactosaemia):
Galactose build up
Galactosuria (above renal threshold)
Galactose -> Galactitol (aldose reductase/NADPH)
Reduced NADPH = cysteine residues not maintained = cataracts
High Galactose & Galactitol have osmotic effects on eye = glaucoma

Galactose 1 P uridyl transferase (classical galactosaemia):
Galactose 1P build up
Toxic to hepatocytes = jaundice, vomiting

Epimerase:
Prevents transfer of UDP between glucose & galactose
(So cannot convert galactose 1 P to glucose 1 P, which is fed into glycolysis)

37
Q

Anaemia:

Definition/process
Types

A

Reduced no rbc’s / reduced amt O2 reaching organs/tissues

Many diff types:
Blood loss: GIT ulcers etc
Excess breakdown: sickle cell
Deficient release of rbc’s: poor heamatopoiesis

38
Q

Gestational diabetes:

Process

A

During pregnancy, rate of insulin secretion & synthesis increases
If pancreas fails to respond to demands of pregnancy, less insulin than required released
Loss of metabolic control: increased blood glucose = diabetes

Normally reverses after birth
But increased chance of future diabetes

39
Q

Hypercalcalcaemia:

Process
Presentation
Consequences of chronic increased levels of calcium
Treatment

A

Increased PTH (hyperparathyroidism)
PTH related peptide, from cancer
Excess calcitrol?

Stones (kidney stones/damage)
Moans (tiredness, depression)
Groans (abdo pain, constipation)
Bone loss (when due to excess PTH)

Replace fluid
Remove tumour from PTH

40
Q

Hypocalcaemia:

Consequences chronic reduced calcium levels
Causes

A

Hyper-excitability of the NS:
Parasthesia
Tetany/convulsions
Paralysis (death if paralysis diaphragm)

Hypoparathyroidism (rare)
Removal of PT gland
Vit D & calcium deficiency
(When due to diet, not PTH: Ca maintained at expense of bone = rickets in children)

41
Q

Type 1 Diabetes Mellitus:

Definition
Clinical presentation (incl biochem)
Treatment

A

Complete autoimmune destruction of beta cells of pancreas =
no insulin production

Normally younger person
Often post viral infection
Triad: polyuria, polydipsia, unexplained weight loss
Hyperglycaemia: rbg >11.1, fbg >7.0
Ketone body production (noticed in urine/on breath): ketoacidosis

Immediate subcutaneous insulin
Patient education

42
Q

Ketoacidosis:

Cause (& process)
Leading to…

A

T1DM:
Lack insulin
Metabolism of FAs
Increased ketone body production (noticed in urine/on breath)

Hyperventilation
Nausea
Vomiting
Dehydration
Abdo pain
43
Q

Leptin deficiency:

Normal function of leptin
Consequences of deficiency

A

Hormone that controls appetite:
Inhibits stimulatory / stimulates inhibitory neurone

Obesity (therefore a key hormonal target in managing obesity)

44
Q

Type 2 Diabetes Mellitus:

Definition
Clinical presentation
Treatment

A

Gradual destruction beta cells of pancreas
With tissue insulin resistance

Normally older person, obese/overweight
Gradual onset
Triad: polyuria, polydipsia, weight loss (less noticeable)
Hyperglycaemia
Usually no ketone production
Diet & exercise initially
Non-insulin therapies 
(sulphonylureas: increase insulin release/reduce insulin resistance, 
metformin: reduce gluconeogenesis)
Insulin treatment
45
Q

Diabetes:

Macrovascular problems
Microvascular problems
Management

A

MI
Stroke
Poor circulation

Neuropathy
Nephropathy
Retinopathy
Diabetic foot

Monitory with HBA1C every 3m:
Non-enzymatic glycosylation test

46
Q

Lactic acidosis:

How/why occurs
Consequences
Clinical presentation

A

Increased lactate produced in cells
Anaerobic exercise:
Reduction of pyruvate (via lactate dehydrogenase)
Supplies more NAD+ to maintain ATP production

If proton conc in blood > blood buffering capacity = reduced pH
(Excess protons dont come from lactic acid)

Deep breathing, abdo pain, nausea)

47
Q

Metabolic syndrome:

Prevalence
Diagnosis/clinical presentation

A

12-25% (developed countries)

W:H ratio >0.9 (men), >0.85 (women)
BMI > 30kg/m2
BP > 140/90 mmHg
Triglycerides >1.7mM
HDL < 0.9mM (men) 7.8mM
Glucose uptake lowest quartile
48
Q

Cushings:

Definition
Causes
Consequences
Test

A

Increased secretion glucocorticoids (zona fasciculata) =
increased cortisol

Adrenal cortex increased activity
Pituitary: increased ACTH secretion
Ectopic tumour (adenoma in pituitary): increased ACTH secretion

Increased proteolysis (thin arms/legs)
Increased gluconeogenesis
Hyperglycaemia (polyuria/polydipsia)
Lipogenesis (moon face, buffalo hump, weight gain)
Hypertension (increased production mineralocorticoid)
Acne (immunosuppressed)

Dexamethasone suppression test (synthetic steroid)
Normally reduce ACTH & therefore cortisol
Suppression >50% indicates cushings
(Retains some sensitivity; distinguishes from tumours)

49
Q

Addison’s Disease:

Definition
Causes
Clinical presentation
Test
Treatment (Addisonian crisis - worsened by stress)
A

Reduced activity adrenal cortex

Autoimmune destruction adrenal cortex
(reduced glucocorticoids & mineralocorticoids)
Pituitary/hypothalamic disorder
(Reduced ACTH/CRF release)

Insidious onset: weight loss, tiredness, anorexia, abdo pain
Hypotension
Muscle weakness & dehydration
Hypoglycaemia
Increased pigmentation (ACTH acts as MSH: both POMC derived)

Synacthen (synthetic analogue of ACTH)
Normally increases cortisol
Normal response excludes Addisons

Cortisol
Fluid replacement

50
Q

Hyperammonaemia:

Definition
When can occur
Consequences

A

Increased amount of ammonia in blood (NH3+)

High protein diet & partial urea cycle deficit
Amino acid metabolism deficit
Re-feeding syndrome (reduced urea cycle from reduced food, rapid re-intro of food, excess aa degradation, reduced urea cycle activity to dispose of ammonia)

Toxic to CNS (tremors, slurred speech, coma, death)
Increased blood pH
Reacts with alpha ketoglutarate; removes TCA substrate = reduced energy supply

51
Q

Phenylketoniria (PKU):

Definition
Consequence (process, clinical)
Test
Treatment

A

Inherited condition: defective enzyme phenylalanine hydroxylase

Prevents conversion phenylalanine -> tyrosine (used to make hormones & neurotransmitters; noradrenaline, adrenaline, dopamine, as well as thyroid hormones)
Build up phenylalanine; drives alternative path- converted to phenylpyruvate
Lack of neurotransmitter synthesis (phenylpyruvate prevents pyruvate uptake to mitochondria: brain energy metabolism)
Can cause mental retardation (phenylalanine inhibits brain dev)

Heel prick test @ birth

Diet low in phenylalanine
Tyrosine supplements

52
Q

Uncouplers:

Process
2 causes (unnatural, natural)
A

Increase permeability of inner mitochondrial membrane to protons
Uncoupling ETC from Oxidative Phosphorylation
Dissipation of p.m.f. As heat
Protons bypass ATP synthase

Pesticide poisoning (e.g. dinitrocresol, dinitrophenol)
Brown adipose tissue via UCP-1: allows non shivering thermogenesis
53
Q

Cyanide poisoning:

How works
Process

A

Blocks ETC

Binds to electron transport proteins
Prevents oxidation NADH & FAD2H
Prevents ETC initiating
No free energy released by REDOX reactions of ETC
= proton translocation complexes unable to pump protons into intermembrane space
Prevents establishment of p.m.f.

54
Q

Glycogen storage disease:

Consequences: too much / too little

A 
Too much:
Tissue damage (liver, musc)

Too little:
Poor exercise tolerance
Fasting hypoglycaemic tendencies

55
Q

Hyperglycaemia:

Clinical presentation (on testing)

Tests & thresholds

A

Glucose in urine; above renal threshold
Polyuria, polydipsia (osmosis)

Random blood glucose > 11.1 mM
Fasting blood glucose > 7.0 mM
Non-enzymatic glycosylation of proteins (HbA1C) >10% (normal 4-6)
Plasma glucose 2 hrs after OGTT >11.1 mM

56
Q

Hypoglycaemia:

Test & threshold
Consequences
Clinical presentation

A

Blood glucose conc < 3.0 mM

Can be rapidly fatal: glucose essential for CNS function

Slurred speech
Reduced coordination
Dizziness/headache
Coma
Death
57
Q

Excess paracetamol:

Normal metabolism
Metabolism after toxic dose
Treatment

A

Normally straight to phase 2 metabolism

Phase 2 metabolism saturated so induces phase 1:
Phase 1 Creates toxic intermediate (NAPQI): toxic to hepatocytes
Phase 2 conjugation with glutathione (reduces ROS defences)

Activated charcoal to reduce adsorption / N-acetyl cysteine

58
Q

Lactose intolerance:

Enzyme deficiency
Consequence
Clinical presentation (& explanation)
Treatment

A

Lactase

Lactose cant be broken down; remains in gut

Stomach cramps, diarrhoea (water drawn in to lumen of colon by osmosis)
(Bacteria colonise un-hydrolysed lactose; ferments to produce organic acids: irritate GIT)

Lactose free diet (avoid most dairy products)

59
Q

Homocystinuria:

Definition
Cause
Clinical presentation
Treatment

A

Inherited condition; defect in CBS enzyme

Build up of methionine & homocysteine (from breakdown of aa’s that cannot then be converted to cysteine)
Affects Fibrillin-1 protein structure
(Stretchy skin; affect on CT - similar to Marfans, chest pain, dev delay; methionine)

Low methionine diet
Vit B6 to increase remaining CBS activity

60
Q

Glucose 6 phosphate dehydrogenase deficiency:

What this enzyme does
Consequences of deficiency

A

Oxidise G6P; responsible for pentose phosphate pathway
(Produces 5C ribose sugars for nucleotide synthesis in actively dividing tissues, produces NADPH)

Reduction in NADPH =
Reduced lipid synthesis
Reduced maintenance of SH residues in lens of eye = cataracts
Reduced maintenance of SH residues in rbc’s = disulphide bonds form (Heinz bodies)
Prevents glutathione reduction: important in rbc’s etc for ROS detox

61
Q

Hyperlipidaemia:

Definition
Cause
Clinical presentation
Treatment

A

Increased triglyceride lvl in blood (often after fatty meal)
Increased chylomicrons in blood many hrs after meal (lack of breakdown)

Defect in lipoprotein lipase

Abdo pain

Low fat diet

62
Q

Marasmus:

Kind of deficiency
Where seen/what population
Clinical presentation (& explanation)
Why proteins need to be reintroduced slowly
A

Calorific & protein deficiency

Young children/developing world

Muscle wasting, emaciated, loss body fat, no oedema
(Fat metabolised to make ketones in liver, but need lipoproteins to transport ketones, therefore breakdown muscle)
SOB, tachycardic
(Not enough water to maintain BP)

Protein broken down in liver to lipids
But no protein to transport out = fatty liver

63
Q

Kwashiorkor:

Kind of deficiency
Clinical presentation (& explanation)
Why need to re-introduce food slowly
A

Low protein, adequate calories

Ascites & oedema
(Low oncotic pressure because low serum protein production e.g. Albumin; water out to tissues & not returning)
Hepatomegaly
(Lack aa’s for transport proteins, less fat transport, fat builds up in liver, less fat breakdown)
Thin limbs

Liver damage = urea cycle not working well: toxic ammonia not converted to urea
No albumin stores = inadequate colloid pressure = water not drawn out = oedema

64
Q

Jaundice:

Process that causes

A

Damage to liver
Broken down rbc’s = Hb = heme = bilirubin
Less bilirubin conjugated (made water soluble) by liver
Unconjugated bilirubin builds up & released into blood
Insoluble therefore moves into tissues
Brown/yellow unconjugated bilirubin in blood & tissues = jaundice

65
Q

Familial hypercholesterolaemia:

Cause
Clinical presentation
Treatment

A

Absence/deficiency of LDL receptors = increased LDL & cholesterol kn blood

Xanthelasma
Corneal arcus
Increased atherosclerosis (LDLs -> cholesterol deposit -> plaque)

Lifestyle changes (diet, exercise)
Statins (inhibit HMG CoA reductase)
66
Q

Obesity:

BMI: clinical & morbid obesity
Causes
Treatments
A risk factor for…

A

> 30
35

Excessive energy intake (increased fat, alcohol)

Exercise
Reduce fat content

T2DM
CHD: atherosclerosis
Oesteoarthritis
Cancers
Psychological damage
67
Q

Oxidative stress:

Definition
Poss causes
Management

A

Antioxidant levels too low to deal with ROS levels

G6P-dh deficiency
(Normally Reduces glutathione: key part of defences)
Superoxide dismutase deficiency
Catalase deficiency
(Both deficiencies = reduced superoxide radicals)

Important in many disease states e.g. alzheimers)

Increase antioxidants e.g. Fruit

68
Q

Excess alcohol (chronic):

Consequences
Treatment

A

Acetaldehyde can increase sufficiently to cause liver damage
Reduced NAD+/NADH ratio: affects many normal liver processes incl gluconeogenesis
Increased FA synthesis & reduced lipoprotein (fatty liver)
Loss enzymes in cells due to leakiness
GI disturbances

Disulfiram:
Inhibits aldehyde dehydrogenase causing ‘hangover’ which can inhibit alcohol dependency

(Alcohol -> acetaldehyde -> acetate -> acetyl coA)
(Alcohol dh, aldehyde dh)
(Also reduced NAD+ to NADH, ATP to AMP)

Clinical Conditions (3 decks)

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