Body Log Flashcards
Dehydration
Causes
Mode of action
Symptoms
Treatment
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
Oedema
What is it
Mode of action
Causes
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,
Hyperthyroidism
What is it
Levels of antibodies
High levels of T3 or T4
Low TSH
Hypothyroidism
What is it
Levels of hormones
Low T3 and T4
High TSH
Parathyroid disease
What is it
Symptoms
Over production of PTH from a parathyroid tumour leading to high blood calcium
Causes symptoms of the brain, muscles and bones
Liver fibrosis
Pathophysiology
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
In which diseases are ANP and BNP released?
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)
Scurvy
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
Ectopic pregnancy
Implantation of embryo in Fallopian tube leads to rupture of tube= miscarriage and haemorrhage
Placenta praevia
Implantation of embryo in lower segment of the uterine wall placenta blocks cervix
C-section required due to risk of haemorrhage
Marfan’s syndrome
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)
Ellen’s-Danlos disease
Type 3 collagen deficiency leading to loss of structure
Presents as stretchy skin, unstable joints, easy bruising
Allopecia areata/universalis
Autoimmune destruction of hair follicles
Can occur anywhere and everywhere
Worsened by stress
Psychosocial problems particularly for women
Vitiligo
Autoimmune destruction of melanocytes leads to depigmentation
Psychosocial problems for dark-skinned people ( not very noticeable on fair skin)
Psoriasis
Extreme overproduction of skin cells leading
Treat with steroids
Malignant melonma
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)
Osteogenesis imperfecta
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
Rickets
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
Achondroplasia
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
Myasthenia Gravis
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
Botulism
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)
Hypoparathyrodism
Lack of PTH= lack of calcium absorption= seizures
Multiple sclerosis
Autoimmune destruction of myelin sheath and Schwann cells = decrease in conduction- loss of function
Treatment: B interferon or steroids
Compartment syndrome
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
Muscle hypertrophy
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
Duchess muscular dystrophy
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
Organophosphate poisoning
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
Osteoarthritis
Age related
Degeneration
Mechanical failure of the articular cartilage- narrowing of the joint space- bone rubs against bone
Rheumatoid Arthritis
Autoimmune disease
Inflammation of synovial membrane
= thickening of the joint capsule
Subsequent damage to underlying bone and articular cartilage - both bone and cartilage disintegrate
Osteoarthritic knee joint
Degeneration of the cartilage
Narrowing of the joint space
Growth of bony spurs (osteophytes)- causes inflammation and pain
Osteomalacia
Osteomalacia:
Vitamins D deficiency = lower mineralisation, increased osteoid
Osteoporosis
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
Sentinel lymph nodes
First node to receive lymph form primary tumour
Cancer cells travel through newly produced vasculature, interstitial space and lymph
=swelling of lymph nodes
Primary Lymphodema diseases
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
Secondary lymphoedema
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
Psoriasis
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
hyperkertosis
Too much keratin put on the surface of skin (especially on the hands and feet)
Multiple sclerosis
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
