Mbbs Ii - S2 Exam Study

Front 1

What is heart failure?

Back 1

A syndrome characterised by inability of heart to maintain output sufficient for the metabolic requirements of the body in the presence of a normal filling pressure.

Front 2

Main factors influencing stroke volume (SV)

Back 2

1) Preload: end-diastolic fibre length
2) Contractility of muscle fibers (controlled by neurohumoral mechanisms)
3) Afterload: resistance against which fibres must contact to expell blood

Front 3

What are some compensatory mechanisms in early CCF?

Back 3

1) Increased sympathetic activity
2) Salt & water retention by kidney
3) Myocardial hypertrophy +/- dilation

Front 4

Systolic v diastolic dysfunction

Back 4

Syst. Dys. - Occurs due to an increase in afterload (secondary to e.g. aortic stenosis / systemic HT) leading to concentric hypertrophy, ischaemic myocardium & ultimately impaired contractility.

Dias. Dys. - Decrease in preload leading to decreased SV. Is caused by obstruction to LV filling (e.g. mitral stenosis / tamponade) or certain arrythmias which limit filling time.

Front 5

What is stroke? What are it's main causes?

Back 5

Sudden onset of non-traumatic focal neurological deficit that causes death or lasts for over 24 hours, irreversible damage to neurological tissue.

Cerebral infarction (85%), Intracerebral haemorrhage (10%)

Front 6

What is aphasia?

Back 6

Loss of capacity for communication by speech, writing or signs due to lesion of dominant hemisphere. (Broca’s aphasia - abnormal speech, normal comprehension. Wernike’s aphasia - normal speech, abnormal comprehension)

Front 7

What is dysarthria?

Back 7

A disturbance of speech / articulation due to emotional stress, to brain injury, or to paralysis, in-coordination, or spasticity of the muscles used for speaking.

Front 8

What is Methylphenidate's (Ritalin) mechanism of action? AE?

Back 8

MOA: Norepinephrine and dopamine reuptake inhibitor. It blocks the dopamine transporter.

AE: Psychosis, difficulty sleeping, mood swings,stomach aches, diarrhoea, headaches, increased sex drive

Front 9

What is the first-line hypoglycaemic for type-II diabetics & how does it work? AE/CI's?

Back 9

Metformin;
1) Reduces hepatic gluconeogenesis
2) Decreases absorption of glucose from GIT
3) Increases peripheral uptake & utilization of glucose.

AE: Diarrhoea, cramps, nausea, vomiting
CI's: CHF

Front 10

Name a Suphonylurea, its MOA, AE & CIs

Back 10

Glibenclamide

MOA: Bind to an ATP-dependent K+ channel on the cell membrane of pancreatic beta cells. Depolarization -> Voltage-Gated Ca++ channels open -> Ca++ influx -> Insulin exocytosed.

AE: Weight gain,GIT symptoms, headache

Contraindications: Teratogenic, thus cannot be used in pregnant patients

Front 11

Name an acarbose drug, its MOA, AE & CIs

Back 11

Glucobay

MOA: Inhibits alpha-glucosidase enzymes in the brush border of the small intestines and pancreatic alpha-amylase to prevent conversion of carbs to glucose & thus absorption.

AE: Flatulence, diarrhoea, abdominal cramping

Contraindications: IBD, GIT ulceration / obstruction

Front 12

Name one of the Glitazones, its MOA, AE & CIs

Back 12

Rosiglitazone

MOA: Bind to PPAR inside the cell nucleus
1) Decrease insulin resistance
2) Inhibit VEGF
3) Decrease leptin
4) Increase adiponectin levels

AE: Hepatitis, disruption of liver enzymes, weight gain.

Contraindications: Liver disease, CHF, IHD.

Front 13

What is Carbimazole? What is its MOA? Its AEs?

Back 13

Anti-Thyroid

MOA: Prevents the peroxidase enzyme from coupling and iodinating the tyrosine residues on thyroglobulin, hence reducing the production of the thyroid hormones T3 and T4.

AE: Rashes, pruritus (itch), rarely it may cause bone marrow suppression

Front 14

Selective Serotonin Reuptake Inhibitors (SSRIs) - Example, MOA, AE/CI

Back 14

Sertraline

MOA: Binds to 5-HT transporters.

Selectively prevents the reuptake of serotonin into presynaptic cell

AE: GI symptoms, insomnia, agitation, sexual dysfunction.

Containdications: Other Anti-depression drugs, beta-blockers, antiarrhythmic agents.

Front 15

Serotonin-NorepinephrineReuptake Inhibitors (SNRIs) - Example, MOA, AE/CI

Back 15

Venlafaxine

MOA; Acts on 5-HT & norepinephrine transporters in presynaptic bulb to prevent reuptake & prolong their effect in synaptic cleft.

AE: Nausea, drowsiness, loss of libido & orgasm

Contraindications:
HT, IHD, High risk of stroke, other ADDs

Front 16

Tricyclic Antidepressants (TCAs) - Example, MOA, AE/CI

Back 16

Amitriptyline

MOA: Non-selective - Inhibit the reuptake of the neurotransmitters norepinephrine and serotonin by neurons. May also possess an affinity for muscarinic and histamine H1 receptors to varying degrees. Increase amine transmitters in synaptic cleft.

AE: Reduced secretions, postural hypotension, heart symptoms, sedation, hyperthermia

Contraindications:
Alcohol, cardiac conditions, ADDs

Front 17

Monoamine Oxidase Inhibitors (MAOIs) - Example, MOA, AE/CI

Back 17

Selegiline

MOA: Inhibits the activity of monoamine oxidase preventing the breakdown of monoamine neurotransmitters, which increases their availability.

AE: Induce hypertension, liver damage

Drug Interactions:
Sympathomimetics, anticholinergics, antihistamines, opioids, alcohol, barbiturates, methamphetamines, migraine drugs, other ADDs

Front 18

What is Phenytoin (IV) & Carbamazepine used for? MOA, AE/CIs?

Back 18

First-line antiepileptic, used in the treatment of seizures.

MOA: Dampens brain activity seen in seizure by reducing electrical conductance among brain cells by stabilizing the inactive state of voltage gated sodium channels.

AE: Sedation, reduced cognitive function, nystagmus, paradoxical seziures, teratogen (reduces folic acid levels)

CI: Pregnancy

Front 19

What is Valproic Acid / Valproate? MOA, AE/CIs?

Back 19

Anti-convulsant & mood stabilizing drug.

MOA: Blocks transamination of GABA, blocks the voltage-gated sodium channels and T-type calcium channels.

AE: Dyspepsia, sedation

CI: Pregancy (teratogenic)

Front 20

What is Lamotrigine (Lamictal)? MOA, AE/CIs?

Back 20

Anti-convulsant & mood stabilizing drug.

MOA: Inhibits voltage-sensitive sodium channels, thereby stabilizing neuronal membranes & modulating presynaptic transmitter release of excitatory amino acids (e.g. glutamate and aspartate)

AE: Toxic Epidermal Necrolysis, Stevens-Johnson syndrome, headaches, sedation, reduced cognitive function

Front 21

Name the drug which mimics the chemical structure of the neurotransmitter gamma-aminobutyric acid (GABA)

Back 21

Gabapentin (Neurontin) - antiepileptic & neuropathic pain reliever

Front 22

What is Methadone? MOA, AE/CIs?

Back 22

Synthetic Opioid

MOA: Full mu-opioid agonist. Also binds to the glutamatergic NMDA (N-methyl-D-aspartate) receptor, and thus acts as a receptor antagonist against glutamate.

AE: hypoventilation, constipation, miosis, nausea, itching, insomnia

Front 23

Name an osmotic diuretic. MOA, AE/CIs?

Back 23

Mannitol

MOA: Is a polyol (sorbitol stereoisomer) filtered in PCT but not reabsorbed.

AE: Acidosis (if not given with IV bicarb)

CI: CCF

Front 24

Name a loop diuretic. MOA, AE?

Back 24

Furosemide (Most commonly used drug in CCF)

MOA: Acts by inhibiting Na+/K+/2Cl- symporters in the thick ascending limb, greatly reducing Na+ reabsorption.

AE: Electrolyte imbalance

Front 25

Name a potassium sparing diuretic (aldosterone agonist). MOA?

Back 25

Spironolactone

MOA: Competitive inhibition of mineralocorticoid receptors in DCT, prevents the binding & subsequent effect of aldosterone.

AE: Hyperkalaemia

Front 26

Name a thiazide diuretic. MOA, AE?

Back 26

Hydrochlorothiazide

MOA: Inhibits Na+/Cl- symporter on luminal surface of cells in the early DCT.

AE: hypokalemia, increased serum cholesterol, triglyceride, IGT.

Front 27

Name a calcium channel blocker. MOA?

Back 27

Amlodipine

MOA: Blocks voltage-gated calcium channels (VGCCs) in muscle cells of the heart and blood vessels. Leading to ↓ cardiac contractility → ↓CO. In blood vessels, a decrease in calcium results in less contraction of the vascular smooth muscle → vasodilation → ↓TPR

Front 28

What is Digoxin? What is it's MOA, AE/CIs?

Back 28

Cardiac glycoside + Antiarrhythmic

MOA: Binds (inhibitively) to a site on the extracellular aspect of the α-subunit of cardiac Na+/K+ pump → ↑ intracellular Na+ → Disruption to Na+ gradient slows down extrusion of Ca2+ by the Na+/Ca2+ pump.

AE: loss of appetite, nausea, vomiting, diarrhea, blurred vision, visual disturbances (yellow-green halos), confusion, drowsiness, dizziness, nightmares, agitation, and/or depression, as well as a higher acute sense of sensual activities

CI: Hydroxychloroquine

Front 29

What is Warfarin? What is it's MOA, AE/CIs?

Back 29

Anticoagulant

MOA: Inhibits enzyme epoxide reductase blocking vitamin K metabolism

AE: Hemorrhage, osteoporosis

CI: PUD, Concurrent NSAIDs, Recent intracranial haemorrhage, cirrhosis, advanced malignancy, recurrent falls.

Front 30

What is Amiodarone?

Back 30

Antiarrhythmic (Most effective currently available)

MOA: Actions on the SA and AV nodes.
1) Increases the refractory period via Na+/K+ channel effects
2) Slows intra-cardiac conduction of the cardiac action potential, via Na+channel effects.

AE: thyroid effects (common), intestital lung disease (uncommon)

CIs: anaphylaxis, pregnancy/breastfeeding

Front 31

Risk factors for CCF

Back 31

Hypertension (HT)
Myocardial infarction (MI)
Valvular heart disease
Viral myocarditis
Bacterial endocarditis
Alcohol
Persistent tachycardia
Anaemia
Iron (Fe) overload
Thyroid disease
Amyloidosis

Front 32

What is ejection fraction? What investigation is commonly used to determine EF?

Back 32

Fraction of blood pumped out of a ventricle with each heart beat.
SV / EDV
or
(EDV - ESV) / EDV

Echocardiography

Front 33

What is acetylsalicylic acid more commonly known as? MOA, AE/CIs?

Back 33

Asprin (NSAID, analgesic, antipyretic, antiplatelet)

MOA: Inhibits both the cyclooxygenase-1 (COX-1) and cyclooxygenase-2 (COX-2) isoenzymes.

AE: GI ulcers, tinnitus

CI: Haemophilia

Front 34

What is FEV1, FVC, FEV1/FVC in obstructive vs restrictive airways disease?

Back 34

Obstructive:
FEV1 - decreased
FVC - decreased or normal
FEV1/FVC - decreased

Restrictive:
FEV1 - decreased or normal
FVC - decreased
FEV1/FVC - increased or normal

Front 35

What are the 3 main systems regulating blood acid-base balance? Timeframe?

Back 35

(1) Chemical acid-base buffer systems of body fluids
• Acts within a fraction of a second
• Is a means of compensation until balance can be re-established
(2) Respiratory center
• Second line of defence
• Acts within a few minutes to eliminate (or reduce elimination of) CO2
(3) Kidneys
• Acts slowly (hours to days)
• By far the most powerful of the acid-base regulatory systems

Front 36

List the factors that increase H+ secretion and HCO3- .reabsorption by the renal tubules.

Back 36

↑ Pco2
↑ H+, ↓HCO3-
↑ Angiotensin II
↑Aldosterone
↓ Extracellular fluid volume
Hypokalemia

Front 37

List the factors that decrease H+ secretion and HCO3- reabsorption by the renal tubules

Back 37

↓ Pco2
↓H+, ↑HCO3-
↓Angiotensin II
↓Aldosterone
↑Extracellular fluid volume
Hyperkalemia

Front 38

What is considered normal pH, H+, Pco2, HCO3-?

Back 38

pH 7.4
H+ 40 mmol/L
Pco2 40 mmHg
HCO3- 24 mmol/L

Front 39

For which condition are eczema, allergic rhinitis, parental history of atopy, smoking or living with smokers (childhood) important risk factors for?

Back 39

Asthma

Front 40

What is asthma?

Back 40

A chronic inflammatory disorder of the airways in which many cells and cellular elements play a role, in particular, mast cells, eosinophils, T lymphocytes, macrophages, neutrophils, and epithelial cells.

Front 41

What are 4 key clinical features of asthma?

Back 41

Wheeze
Chest tightness
SOB
Cough

Front 42

What is hypersensitivity?

Back 42

- Immune system responds excessively or inappropriately to an antigen
- Causes pathological changes
- Requires a period of sensitization
- Requires breakdown of peripheral tolerance

Front 43

List some of the pathological hallmarks of asthma.

Back 43

Smooth muscle hypertrophy and hyperplasia
Inflammatory cell infiltration
Oedema
Goblet cell and mucous gland hyperplasia
Mucus hypersecretion
Protein deposition including collagen
Epithelial desquamation

Front 44

What are the 4 main classes of "preventer" drugs used in the treatment of asthma? Provide an example of each.

Back 44

1. Corticosteroids
- Inhaled (Belomethesone)
- Oral (Prednisolone)
2. Cranolyns (sodium chomolycate)
3. Oral leukotriene receptor antagonists (montelukast)
4. Anti-immunoglobulin E therapy

Front 45

What are the 3 main classes of "reliever" drugs used in the treatment of asthma? Provide an example of each.

Back 45

1. Short-acting beta-adrenoceptor agonists SABA (Salbutamol)
2. Long-acting beta-adrenoceptor agonists LABA (Salmeterol)
3. Anticholinergic drugs
i. Short acting (ipetrium bromide)
ii. Long acting (liotropium)

Front 46

What is the mechanism of action of corticosteroids in the treatment of asthma? AE?

Back 46

Cortisol binds to intracellular receptors →interaction with DNA → synthesis of lipocortin → inhibits phospholipase A in cell membrane → inhibits production of inflammatory mediators (prosoglandins, eosinophils) → inhibits IgE synthesis, ↓mucus secretion, ↓eicosonoide generation, up-regulation of ß receptors → smooth muscle relaxation → bronchiolar dilation

AE: growth delay in children (?), adrenal suppression at high doses, hoarse voice and oral thrush (inhaled)

Front 47

What is the mechanism of action of Salbutamol in the treatment of asthma? AE?

Back 47

Stimulates ß2 receptors on airway smooth muscle → stimulation of G protein → adenyl cyclase activation → ↑intracellular cAMP relaxes smooth muscle cells → bronchodilation

Also intracellular cAMP → inhibition of mast cell mediator release → inhibition of plasma exudation & airway oedema

AE: tremor, cardiac rhythm disturbances, nausea and vomiting

Front 48

What is the mechanism of action of ACh drugs in the treatment of asthma? AE?

Back 48

Bind to muscarinic receptor in airways smooth muscle → inhibits constricting parasympathetic effects of Ach → ↓mucus secretion & bronchodilation

AE: Dry mouth (well tolerated)

Front 49

What is the MOA of prolactin & oxytocin?

Back 49

prolactin → portal circulation → stimulates breast glandular alveoli → ↑ milk production

oxytocin → systemic circulation → acts on subareolar smooth muscles → stimulates contraction of myoepithelial cells → lactiferous sinuses → lactiferous ducts → milk ejection

Front 50

What are oestrogen's 3 main effects on the breast?

Back 50

1) Development of stromal (CT) tissues
2) Growth of duct system
3) Deposition of fat in breasts

Front 51

What are progesterone's 3 main effects on the breast?

Back 51

1) Development of lobules and alveoli of the breasts.
2) Alveolar cell proliferation, enlargement and conversion to becoming secretory in nature
3) Breast swelling (secretory development -> fluid in subcutaneous tissue)

Front 52

What % of all breast cancers are in situ? What are the 2 main types? What's the breakdown?

Back 52

In Situ Carcinoma -15-30%
1) Ductal carcinoma in situ (DCIS) 80%
2) Lobular carcinoma in situ (LCIS) 20%

Front 53

What % of all breast cancers are invasive? What are the 2 main types? What's the breakdown?

Back 53

Invasive Carcinoma - 70-85%
1) No special type carcinoma ("ductal") 79%
2) Lobular carcinoma 10%

Front 54

What are the 4 main proto-oncogenes which commonly undergo mutation in breast cancer?

Back 54

BRCA 1
BRCA 2
p53
c-erb B2 / HER-2

Front 55

What is epigenetics? What's it's role in cancer?

Back 55

A change in the pattern of expression without a change in the DNA sequence.

Changes include hypomethylation, dysregulation of DNA methyltransferase I, and hypermethylation.

E.g. Hypermethylation → silencing of tumor suppressor genes → unregulated cell growth.

Front 56

Mutagen v Carcinogen

Back 56

Mutagen: causes a stable change in the DNA, not necessarily causing cancer.

Carcinogen: causes changes in DNA which lead to the development of cancer.

Front 57

Name 3 of the main ways proto-oncogene → oncogene.

Back 57

1) Point mutation in a gene: e.g. ras gene trapped in active form → persistent activation of mitogenic signaling pathway.

2) Translocations: Formation of gene for aberrant protein with growth stimulating activity or alterations in transcription of proto-oncogene

3) Amplifications: extra copies of a proto-oncogene are made→ more protein product. E.g. amplification of c-erb¬ B2 (neu/HER-2) in breast cancer → extra copies of growth factor receptor → over stimulation of breast cell

Front 58

What is the triple test? What is it's sensitivity & specificity?

Back 58

1. Medical history and clinical breast examination
2. Imaging tests
a. Mammography (if >35 y.o.)
b. Ultrasound (if <35 y.o., , pregnant or lactating)
3. Nonsurgical biopsy
a. Fine needle aspiration (FNA) cytology
b. Core biopsy

Has a sensitivity of >99.6% and specificity of >62%

Front 59

What is the sentinel node?

Back 59

The first lymph node that breast cancer cells may spread to outside the breast. (In most cases, the sentinel node is in the armpit / axilla.)

Front 60

Name a first-line selective oestrogen receptor modulator (SERM) drug used in breast cancer. MOA, AE/CIs?

Back 60

Tamoxifen

MOA: Competitively binds to oestrogen receptors on tumours and other tissue targets, producing a nuclear complex that decreases DNA synthesis and inhibits oestrogen effects.

AE: Increased risk of endometrial cancer & thromboembolus menopausal symptoms

CI: OCP

Front 61

Name 2 monoclonal Ab (targetted therapies) commonly used in the treatment of breast cancer & their MOA.

Back 61

1) Traztuzumab - a monoclonal Ab that works against those with the HER-2 oncogene (20% of breast Ca). It opsonises it for destruction by immune system.

2) Gleevec - a small molecule therapy (target receptor tyrosine kinase) that inhibits signal transduction pathway for RAS resulting in downregulation of RAS

Front 62

Risk factors for breast cancer.

Back 62

Gender and age (female, >50yrs)
Previous breast cancer (in same or opposite breast)
Prior breast biopsies, showing atypical cells
Prior neck or chest radiation
History of primary cancer of Ovary, Uterus, Bone or Soft Tissue
Family history of breast cancer
Male in family with breast cancer
Family history of Ovarian cancer
No children or age at first live birth >35yrs
Diet high in animal fat an low in fibre, fruit and vegetables
Obesity(fatty tissue converted to oestrogen)
Early menarche (<11) and late menopause (>55)
High intake alcohol
Smoking
HRT (for 4-5 yrs)
OCP
Higher socioeconomic status
Lack of breast feeding

Front 63

Acute management of pulmonary oedema.

Back 63

LMNOP
L - Lasix (Furosemide)
M - Morphine (venodilator)
N - Nitrate (reduces LV preload)
O - Oxygen (consider CPAP)
P - Position (upright, gravity)

Front 64

2 factors which determine ventilation.

Back 64

1) Airways resistance
2) Lung compliance

Front 65

What is compliance?

Back 65

∆V/∆P
How easy it is to inflate an elastic structure.

Front 66

↑ compliance vs ↓ compliance

Back 66

Lung with ↑ compliance inflates to a greater extent than lung with ↓ compliance

Front 67

How does pulmonary system respond to increase efficiency?

Back 67

1) Recruitment (increase # of open capillaries)
2) Distension (incresae diameter of already open capillaries)

Front 68

What determines flow rate after initial expiration?

Back 68

Natural elasticity of the lung, NOT expiratory muscles.

Front 69

Which 4 factors determine diffusing capacity of gases in alveoli?

Back 69

1) Capillary wall thickness
2) Pressure difference
3) Cross-sectional area
4) Solubility and molecular weight

Front 70

What are the main cytokines of rheumatoid arthritis?

Back 70

1) TNF-α
2) IL-1, IL-4, IL-6, IL-10
3) Interferon-γ

Front 71

Which MHC II genetic variants are strongly linked to rheumatoid arthritis?

Back 71

1) HLA-DR B1*0401
2) HLA-DR B1*0404

Front 72

What is the aetiology of rheumatoid arthritis?

Back 72

Genetic predisposition (HLA-DR) -> arithritogenic peptide presented to T-cells by APC -> acute inflammatory response -> chronic inflammatory response -> pannus formation -> bone & cartilage destruction.

Front 73

Name 6 potential targets for drugs in the rheumatoid arthritis pathway.

Back 73

1) Ag presentation by APC to Tcell
2) Cell migration (chemotaxis)
3) Tcell activation
4) Tcell proliferation (DNA synthesis)
5) Inflammatory mediators
6) Tissue destruction (cartilage/bone)

Front 74

What is rheumatoid factor? In what % of RA patients is it found?

Back 74

A subset of antiglobulin antibodies directed against the Fc region of IgG.

75-80% of RA patients

Front 75

What is anti-CCP?
What is it's sensitivity & specificity for RA?

Back 75

Anti-cyclic citrullinated protein antibodies. Diagnostic marker for RA
Sensitivity for RA 70-80%
Specificity for RA 90-97%

Front 76

What is the first-line DMARD used in RA? MOA, AE,CIs?

Back 76

Methotrexate (Anti-folate)

MOA: Interferes with folic acid metabolism, DNA synthesis, inhibits T-cell proliferation

AE: Anaemia, neutropoenia

CI: Pregancy (Highly Teratogenic)

Front 77

TNF-α inhibitor drug. MOA, AE?

Back 77

Infliximab (Monoclonal Ab)

MOA: Binds to the soluble and transmembrane forms of TNFα and inhibits or prevents the effective binding of TNFα with its receptors.

AE: Immunosuppression

Front 78

glyceryl trinitrate. MOA, AE

Back 78

vasodilator

MOA: Exogenous source of nitrates → venodilation → ↓ venous return & preload on heart → ↓ myocardial O2 requirement (also dilation of arterioles & coronary arteries)

AE: hypotension

Front 79

atorvastatin. MOA, AE, CIs

Back 79

hypolipidaemic

MOA: Inhibit HMG-CoA reductase → interferes with production of mevalonate → blocks cholesterol production in liver

AE: myalgia, mild GI symptoms, headache

CI: pregnancy

Front 80

omeprazole. MOA, AE

Back 80

proton-pump inhibitor

MOA: Inhibits H+/K+-ATPase on parietal cells → inhibition of basal & stimulated acid secretion

AE: headache, nausea, vomiting, diarrhoea/constipation

Front 81

anastrozole. MOA, AE

Back 81

aromatase inhibitor

MOA: (in post-menopausal women): inhibit conversion of circulating androstenedione & testosterone to oestriol & oestradiol → reduce tissue oestrogen concentration

AE: Menopausal symptoms

Front 82

alendronate. MOA, AE, CIs

Back 82

bisphosphonate

MOA: inhibit osteoclasts → decrease bone resorption

AE: nausea, vomiting, diarrhoea, headache, MSK pain

CIs: hypocalaemia, NSAIDS

Front 83

Which cells make parathyroid hormone (PTH)? Main function of PTH? How?

Back 83

Parathyroid chief cells

Main function ↑ blood calcium
1) Bone: ↑RANKL → ↑osteoclastic activity
2) Kidney: ↑reabsorption of Ca2+ from DCT
3) GIT: ↑Vitamin D → ↑Ca2+ absorption

Front 84

Which cells make Calcitonin? Main function of Calcitonin? How?

Back 84

Parafollicular / c-cells

Main function ↓ blood calcium
1) Bone: Inhibits RANKL → ↓osteoclastic activity
2) Kidney: ↓reabsorption of Ca2+ & phosphate from DCT
3) GIT: ↓Vitamin D → ↑Ca2+ absorption