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Diseases > Body Log > Flashcards

Body Log Flashcards

1
Q

Dehydration

Causes
Mode of action
Symptoms
Treatment

A

Causes: Hot humid weather, excessive sweating, vomiting, diarrhoea, burns

Mode of action: water loss causes increase in osmolarity and increase in ADH. This decreases plasma volume

Symptoms: olliguria, thirst, dryness

Treatment: fluids

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2
Q

Oedema

What is it
Mode of action
Causes

A

Fluid retention, used to be called dropsy

MOA: hydrostatic pressure being more than osmotic pressure = water moves into interstitial space as there is presence of plasma proteins

Caused by damaged/ blocked lymphatics,

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3
Q

Hyperthyroidism

What is it
Levels of antibodies

A

High levels of T3 or T4

Low TSH

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4
Q

Hypothyroidism
What is it
Levels of hormones

A

Low T3 and T4

High TSH

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5
Q

Parathyroid disease

What is it
Symptoms

A

Over production of PTH from a parathyroid tumour leading to high blood calcium

Causes symptoms of the brain, muscles and bones

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6
Q

Liver fibrosis

Pathophysiology

A

Hepatic stellate cells lose their vitamin A storage capability and differentiation into myofibroblasts

Myofibroblasts synthesis and deposit collagen within the peri sinusoid always space resulting in liver fibrosis

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7
Q

In which diseases are ANP and BNP released?

A

ANP- atrial natriuretic peptide released by atria
BNP- brain-type natriuretic peptide realised by ventricles

Left ventricular hypertrophy, mitral valve (BNP)
Congestive heart failure (ANP)

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8
Q

Scurvy

A

Vitamin C deficiency

Prolyl hydroxylase cannot convert proline to hydroxyproline = reduced H bonds, less crosslinks, weakened structure

Signs and symptoms:
Gum disease
Bruising of skin
Poor wound healing
Bleeding
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9
Q

Ectopic pregnancy

A

Implantation of embryo in Fallopian tube leads to rupture of tube= miscarriage and haemorrhage

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10
Q

Placenta praevia

A

Implantation of embryo in lower segment of the uterine wall placenta blocks cervix
C-section required due to risk of haemorrhage

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11
Q

Marfan’s syndrome

A

Autosomal dominant

Misfolding of fibrillin 1 gene leading to abnormal elastic connective tissue

Signs: very tall, long digits (arachnodactly), high arched palate, joint dislocation

Life expectancy: death round 40 years from aortic rupture (arteries too elastic causing catastrophic haemorrhage)

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12
Q

Ellen’s-Danlos disease

A

Type 3 collagen deficiency leading to loss of structure

Presents as stretchy skin, unstable joints, easy bruising

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13
Q

Allopecia areata/universalis

A

Autoimmune destruction of hair follicles

Can occur anywhere and everywhere

Worsened by stress

Psychosocial problems particularly for women

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14
Q

Vitiligo

A

Autoimmune destruction of melanocytes leads to depigmentation

Psychosocial problems for dark-skinned people ( not very noticeable on fair skin)

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15
Q

Psoriasis

A

Extreme overproduction of skin cells leading

Treat with steroids

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16
Q

Malignant melonma

A

Aggressive skin cancer caused (usually) by excessive UV radiation causing mutations in the melanocytes

If UV penetrates the basement membrane - it metastasises (e.g. brain and liver) poor prognosis

Relatively rare in dark skinned races as melanin protects against UV radiation (evolutionary advantage)

17
Q

Osteogenesis imperfecta

A

Autosomal dominant
Type 1 collagen deformity/deficiency= COL1A gene mutation
major component in ground substance of bone

Severe cases: no conversion of foetal hyaline skeleton= incompatible with life

Most cases: repeated fractures lead to bowed long bones
Hearing loss
Short stature
Hypermobility (loose joints) and flat or arched feet
Poor teeth development
Blue sclera due to unknown cause- possibly thinning of cornea due to issues with collage that forms it

18
Q

Rickets

A

Vitamins D deficiency - not enough sunlight, dietary deficits or decreased ability to convert it
= less absorption of calcium by small bowl causing less rigid bones

Rickets in kids: bowed bones as there are still growing ( epiphyseal growth plates not yet closed after puberty), wears bones, ineffective mineralisation

19
Q

Achondroplasia

A

Autosomal dominant
Deformed fibroblast growth factor - mutation in FGF3 receptor gene leads to decreased endochondral ossification as FGF promotes collagen formation from cartilage
= short limbs, enlarged forehead, normal trunk

20
Q

Myasthenia Gravis

A

Autoimmune destruction of end plate ACh receptors by antibodies = reduced synaptic transmission- reduced endplate invaginations in synaptic clefts

30% reduction in receptor number sufficient for symptoms

Ptosis (drippy eyelids), fatigue, sudden collapse, intermittent muscle weakness

Treatment: immunosuppressive, AChE inhibitors

21
Q

Botulism

A

Botulinum toxin blocks ACh release at motor end plate-= non-contractile state of skeletal muscle- no muscle contraction

Stops facial muscle contraction preventing wrinkles
Treats muscle spasms (e.g cervical dystonia)

22
Q

Hypoparathyrodism

A

Lack of PTH= lack of calcium absorption= seizures

23
Q

Multiple sclerosis

A

Autoimmune destruction of myelin sheath and Schwann cells = decrease in conduction- loss of function

Treatment: B interferon or steroids

24
Q

Compartment syndrome

A

Trauma in one compartment could cause internal bleeding which exerts pressure on blood vessels and nerves

=deep constant poorly localised pain aggravated by passive stretch of muscle group
Paresthaesia (altered sensation)
Compartment feels tense and firm
Swollen shiny skin, sometimes obvious bruising
Prolonged capillary refill time

Treatment: fasciotomy subsequently skin graft

25
Q

Muscle hypertrophy

A

Overstretching- A and I bands can no longer re-engage

= new muscle fibrils are produced, new sacromere are added in the middle of the existing sacromeres

26
Q

Duchess muscular dystrophy

A

Most common muscular dystrophy
X link recessive

Mutation of dystrophin gene
= excess calcium to enter muscle cell
- calcium taken up my mitochondria
- Water taken with it= mitochondria burst
- muscles cells burst (rhabdomyolysis)
- creatine kinase and myoglobin levels are extremely high in the blood

Multiple skeletal muscle related symptoms and sings

Muscle cells replace by adipose tissue

27
Q

Organophosphate poisoning

A

Inhibits the normal function of AChE= ACh activity at NMJ is potentiated

Multiple signs and symptoms
Muscarinic symptoms
S-Salivation
L-lacrimation
U-urination
D- defecation
G-GI cramping
E-Emesis
Nicotinic
M- Muscle cramps
T- tachycardia 
W-weakness
T-twitching 
F-fasciculations
28
Q

Osteoarthritis

A

Age related
Degeneration
Mechanical failure of the articular cartilage- narrowing of the joint space- bone rubs against bone

29
Q

Rheumatoid Arthritis

A

Autoimmune disease
Inflammation of synovial membrane
= thickening of the joint capsule
Subsequent damage to underlying bone and articular cartilage - both bone and cartilage disintegrate

30
Q

Osteoarthritic knee joint

A

Degeneration of the cartilage
Narrowing of the joint space
Growth of bony spurs (osteophytes)- causes inflammation and pain

31
Q

Osteomalacia

A

Osteomalacia:

Vitamins D deficiency = lower mineralisation, increased osteoid

32
Q

Osteoporosis

A 
Primary
type 1 (menopausal)- oestrogen no long mediating osteoclast function
Type 2: old age- loss of osteoblast function- no remodelling, loss of oestrogen and androgen

secondary:
Result of drug therapy
Processes affect bone remodelling
Metabolic bone diseases ( e.g. hyperparathyrodism)

Risk factors:
Insufficient calcium intake
Lack of exercise
Cigarette smoking

33
Q

Sentinel lymph nodes

A

First node to receive lymph form primary tumour
Cancer cells travel through newly produced vasculature, interstitial space and lymph
=swelling of lymph nodes

34
Q

Primary Lymphodema diseases

A

Congenital (Milroy’s disease)
On sent within two years
CauseL mutated FLT4 gene (VEGF-r)
Small or missing endothelial cells in vessel wall

Praecox (Meige’s disease)
Onset: 2-35 years (familial: 1 in 3)
Cause: currently unknown

Tarda
Onset after 35 years
Cause currently unknown

35
Q

Secondary lymphoedema

A

Neoplasia
Pelvic masses
Infiltration of lymph node

Surgery
Node involvement
Accidental

Radiotherapy
Nodal fibrosis- obstruction of vessel

Autoimmune diease
Rheumatoid arthritis
Ezcema

Infection
Cellulitis - obstruction of vessel
Filariasis- parasitic worm that invades and surveys in the lymphatic vessels

36
Q

Psoriasis

A

Extreme overproduction of skin cells- transit time is reduced= stratum corneum is produced in abundance as silvery scales every 2-3 days
Treat with steroids

37
Q

hyperkertosis

A

Too much keratin put on the surface of skin (especially on the hands and feet)

38
Q

Multiple sclerosis

A

autoimmune destruction of myelin sheath and Schwann cells= decrease in conduction leading to loss of function

Symptoms: fatigue, vision problems (diplopia), slurred speech (dysarthria), numbness and tingling sensations (paraesthesia), mobility issues (muscle spasms), urinary retention, constipation

treat with B interferon or steroids

Diseases (8 decks)

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