Radioimmunoassay and Thyroid Abnormalities: Hormonal Analysis and Clinical Insights, Schemes and Mind Maps of Physiology

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. Radioimmunoassay in^ thyroid abnormalites

· RIA is used

for estimation (^) of hormones (^) , (^) proteins , drugs,

and vitamins in^

body funds^

like (^) plasma ,^ wine^ I Of.

· It works on the basis

of competetive^ binding · components especific As (^) (against hormone to be (^) assayed) Radioactively labered^ hormone. · (^) It is^ labelled with -^ peptide hormone :^ radioactive iodine

steroid hormone : Carbon

, (^) Hydrogen Steps :- Radioactive (^) hormone is added to (^) known amount (^) of

Ab

↓ Sample hormone^ competes with^ radioactive^ hormone for Ab^ binding d Bound (^) radioactivity is measured In (^) inyroid hormone : - · B 4are usually measured^ by RIA.

· P Hyperthyroidism : Thyroid hormones 4

TSHA (^) (feedback untibution) ·

1"Hypothyroidism : Thyroid hormones^ I

TSH

· Pitary hyperthyroidism :^ Ts^ , T,^ TSH

9.^ Cretinism · When

hypothyroidism develops^ from or^ before birth

causes :^ -

· Maternal iodine deficiency (^) during pregnancy ·

Maldevelopment of Thyroid gland during

IVL.

· Inborn errors

of thyroid^

hormone (^) synthesis. · Antithyroid Ab (^) (maternal) (^) crossing (^) placenta · Hypopituitarism

Features : - ⑧Ham retard a · dwarf tongue · mentally retarded

way

,Pot^ belly ·

potbelly Menorrhagia

· protrusion of tongue · other # features of hypothyroidism^ · IIIS cold intolerance

· weakness &

fatigue · dry ,^ thick^ skin · hair loss (^) , alopecia · poor (^) memory · inability to^ concentrate · consupation--weight^ gain · thick I husky voice · yellow skin^ (thyronine causes^ arotene

• (^) VitA) S · psychoses (^) - · mennornagea S · unfertility

Treatment

· Important to^ prevent mental^ retardation^ S · (^) i replacement early in

infancy can^ totally^ are^ it

· Usual treatment is prompt treplacement --

&. Role^ of cortisol^

in (^) inflammation · anti-inflammatory &^

anti

Allergic

· Inflammation : response of^ tissue^ to injury Inflammatory responses

· dilation

of capiaries

· (^) increased capillary permeability · migration (^) of granulocytes

to site

of injury

·

killing of pathogen^ (mainly neutrophils

mediators : - S prostaglanders , thrombonanes^ ,^ leukotrienes^ , kinins, histamine (^) , serotonin (^) , lymphokines ,^ Part^ (ptacle^ act factor)

Mechanism :

list inhibits^ synthesis (^) of chemical^ mediators^ ofinfam.- It stimulates (^) synthesis of lipocortins ↓ Tnhibits phopholipase As ↓

Iarachidonic acid^ (precursor

for

mediators

make flowchart first

CORTISOL Lipocortin Stabilises (^) lysosomal Inhibition (^) of most

synthesis membrane^ cel

↓ (^) d (^) ↓ Ophospho- I^ release^ of prote^

• ↓ release (^) of

lipase As^ lytic enupnes histamine

↓ (^) ↓ ↓ Irelease (^) of No (^) proteolytic ↓ vasoditation arachidonic (^) damage ↓ (^) capillary

acid

-^ J^ permeability ↓ ↓^ inflammatory

↓form" of injury

medators on (^) leukocytes ↑ prod of^

IB

d ↓ ↓ (^) chemotanis NF-B remains attached

phagocytosis to^

IkBL

↓ (^) - ↓ Leukocyte activity Inactivation^ of NF-B ↓ Inhibition (^) of gene transcription ↓ ↓ form of^ unflammatory

chemicals

9 .Permissiveaction^ of glucocorticoids · Essential for physiological actions^ of other^ hormones

Calorigenic effects of

Vasopressor (^) GLUCATION &^ CATECHOLS

bronchodilator

F ↑^ -^ Development (^) of effects of mammary gland CATECHOLAMINES (^) Permissive (^) during puberty

Actions

[ -^ lipolitic (^) effects Development (^) of ↓^ of CATECHOLAMINES hepatic enzyme Surfactant^ syn. systems infetal lung maturation of lungs in^ IL Q. Aldosterone^ escape.

· Phenomenon

by which (^) body prevents edema (^) despite (^) high aldosterone levels ↑ (^) salt I water (^) reabsorption by

aldosterone causes Eff

~

expansion

Quenous return^ causing distension^ of atria

d

↑ (^) synthesis I secretion (^) of ANDfrom atrial^ myocytes ↓

profound

natriuresist dirresis

↓

Ect back^ to normal

(iii) Fat^ Metabolism · lipolysis ,

I

plasma level^ of

FFA.

· (^) thus (^) promotes Ketogenesis · so (^) provides

energy in^ hypoglycemia stress

(iv) Electrolyte &^ Water^ Metabolism

influences cone^ of various^ electrolytes :

Plasma ca

by I^ absorption^ from^ 41744VitD effect · Natretention ·^ - mainous Ef volume (^) indirecting (^) by TRAAS (^) & &Ap

· I

plasma (^) phosphate by

reabsorptionfrom proximal tubules g.^ Mechanism^ of insulin^ secretion. · It is influenced (^) by plasma (^) glu come. " ·^ &

When nutrients ↑^. insulin nice versa.

Plasma (^) Glucose n

100 %-^ -

· Linear rise in 50-300mg% Insul seeh · (^) Below 50 mg o^

: nil secretion

500- Above 300

mgolo : (^) no extra so iso (^25050) 7 secretion. Plasma (^) gue

It (^) occurs in I (^) phases

1. First (^) phase (^) response · ↑ (^) plasma (^) gen ⑮ ↓ ↑ (^) uisuin secretion h Reaches (^) peak within^2 mins

↓ to.basal level in next 2-3 mins

· This is the

first I^

rapid (^) phase (^) of insulin^ see"in response to^ plasma (^) glu. · Due to release of already^ synthesied^

I stored^ in^ a

Second Phase (^) Response In the next ⑮ phase, ↑ (^) plasma insulin (^) occurs (^) slonely d reaches peak

in 60 mins

↓

remains elevated

for 3-5h.

· This is second I slow

response

· Due to stimulation

of insulinsyn^

I see"

g.^ Hormones^ of Pancreas · Pancreas (^) is a mixed gland.

• the endocrine part is^ composed^ of clusters^ of cells called Islets (^) of (^) Langerhans ①Insurin secreted (^) by : B cells

Functions :^ -

· anabolic hormone (d blood (^) que) · promotes (^) que uptake into^ muscles^ I^ adiposeissues by ↑^ GLUT4^ activity . · glycogenesis ,^ lipogenesis^ ,^ protein synthesis

Gluconeogenesis ,^ gycogenolysis ,^ lipolysis

Regulation : - +: ↑ (^) bloodgue

,^ aa^ ,^ g1T^

hormones

• : (^) somatostatin I sympathetic Stimulation^ (via^ <re) (ii) (^) Glucagon

secreted

by :^ Xcells functions :^ - · catabolic hormone (^) (4 blood gu) · ⑦

guconeogenesis ,^ glycogenolysis ,^ lipolysis

Regulation :

+: A blood

glu ,^ ↑an^ ,^ Sympathetic^ Stimula^ (viapre)

· - : insulin somatostatin

(ii) Somatomedin

secreted

by : (^) Scells

functions :-

· Paracrine

effect to^ ⑦^ both^ insulin^ /guragon Regulation : - +: ↑ blood (^) que , an (^) , (^) ta · acts as feedback inhibitor^

to maintain normone

balance.

(IV) Pancreatic^ Polypeptide

Secreted (^) by :^ PP^ cells

functions :^ -

· O

pancreatic

enocrine see "

⑨.^ Diabetes^ Mellitus

· Most common endocrine disorder

causes :^ -

· destruction

of cells^

• (^) insulin

deficiency

· I

sensity of insuin^ receptors

· In untreated Am

,^ there^ is^ state^ of starvation^ inthe midst (^) of (^) plenty Pq4- (^) hyperglycemia (^) , but tessie^ cannot^ utilise^ you dre

to insulin

deficiency/resistance^ -^ cellular^ starvation

(i) (^) Neuropathy : (iv) Atheroscleros due to^ I^ plasma IDL (v) Chronic^ ulcer^ &^ diabelie^ foot due^ to^ d^ immunity due^ to hyperglycemia neuropathy . g.^ Cushing^ syndrome ·

hypersecretion of glucocorticoids

causes:^ tumour^ of adrenal^ corten steroid (^) administration

pituitary tumour

adrenal (^) hyperplasia,Humours

features :

(i) (^) Entripetal (^) obesity

· fat is

deposited more^ in^ abdomen^ I^ upper back ·

Buffalo hump^ due^ to^ fat pad^ in^ lower^ week^

I (^) inter scapular (^) region^. (ii) Moon^ face · round faceI red (^) checks

· salt I water retention

(iii) (^) fatigue , weanness (iv) hirswism^ &^ amenorrhea (vi) (^) hypertension · water accumulation (^) (excess glucocorticoids has mincraescorticoid activity .

(vi Reddish^ purple strial on abdomen^ as^ excess^ fat deposi

in (^) abdomen causes stretching (^) of skin.

(i) Exchymoses

· shin I subcutaneous tissueare thin dueto

protein catabolism^. · capillaries on shin (^) become thinI fragile . · so minor injuries cause^ exchymoses^ &^ bruises .

(viii) Proximal^

myopathy · legs become^ thin due (^) to proteolysis inshetal

muscle II bone mass

(iv) Poor^ wound (^) healing ·

hyperglycemia promotes growth oforganism at

wound site

· decreased

immunity

(x) can^ develop hyperglycemia ,

glu intolerance (^) ,^ DM. (i)

Osteoporosis

· ↓ bone mineralisa I d bone (^) mass

9. Hypocalcemic tetany · Hyposecretion of PTH^ is^ common^ following (^) thyroid surgery in^ which^ PTH^ glands^ get accidentary removed Effects :- (i) Chnostek's^ sign :^ quick contraction^ of (^) facial muscles (^) of same

9

. Neurohormonal

reflex

· short term Cardiovascuar

regulatory mechanisms · heep

maintain BP I volume homeostasis

(i) (^) Baroreceptor (^) refeen

· STIMULUS : sudden ↑ord in BP

· RECEPTORS : Carotid Sinus

,^ aorticarch^ (stretch^ receptors) PATHWA : Afferents via (^) IX4X- (^) medullary CV (^) centres

· RESPONSE : 4 BP-d

sympathetic ,parasympathetic

- HARL

vasodilation

BP-sympathetic-4tR , vasoconstriction (ii) Chemoreceptor^ Reflex

· Stimulus :^ do

,^ 4C2^ , Apt

· RECEPTORS : Carotid & Aortic bodies

PATHWAY :^ same

· RESPONSE : respiratory stimulation (iii) CNS^ Eschaemic^ Response

· STIMUWS : Cerebral ischaemia

· RESPONSE : Massive

Sympathetic discharge-^ vasoconstric

• ↑^ BP

(iv) Bainbridge Reflex

· STIMULUS : 4 venous return -

right atrial^ pressure RECEPTORS : Stretch (^) receptors in RA.

· RESPONSE :^ 4 HR wa

vagal

inhibition to prevent ovegiving

⑨. Why are^ exogenously given queocorticoids notslopped

suddenly? · as they supress^ the^

HPA Axis^ I^ sudden withdrawd^ can

cause acute (^) adrenal (^) insufficiency which^ is efe threatening . long term^ geucocortico use^ I^ CrH1^ ACTH d

adrenal glands atrophy I^ stop making cortisol

↓ sudden (^) stoppage - body cannotproduce^ enough^ cortisol ↓ hypotension , (^) hypoglycemia ,^ shock · So , it^ is^ gradually withdrawnto^ allow^ HPA^ anis^ recovery g. Increased^ G-protein activity causes^ acromegaly yproteins ·

Guanine nucleotide^ binding proteins

· molecular switches that mediate

signal transduction · from

R

tointracewar effect ,^ hormonal^ response

Structure

· 3 subunits-L , B , U.

·^ L^ :^ binds (^) GDP (^) &GTP & possesses intrinsic^ GTPase^ activity · B 4V : (^) Stable (^) dimer (^) (BV complex) that^ can^ modulate

effectors