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

An overview of radioimmunoassay (ria) in the context of thyroid abnormalities, detailing its use in hormone estimation and its competitive binding mechanism. It covers various thyroid conditions such as hyperthyroidism and hypothyroidism, along with their hormonal profiles. Additionally, the document discusses the role of cortisol in inflammation, the effects of aldosterone on metabolism, and the mechanism of insulin secretion. It also touches on diabetes mellitus, its types, and complications, as well as calcium and phosphate homeostasis regulated by hormones like pth and calcitonin. The document concludes with a discussion on growth curves, adh function, and thyroid hormone synthesis, offering a comprehensive look at endocrine functions and related disorders. Useful for medical students and healthcare professionals seeking a concise review of endocrine disorders and their diagnostic approaches.

Typology: Schemes and Mind Maps

2023/2024

Available from 06/02/2025

nehanjali-khatiwada
nehanjali-khatiwada 🇮🇳

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Download Radioimmunoassay and Thyroid Abnormalities: Hormonal Analysis and Clinical Insights and more Schemes and Mind Maps Physiology in PDF only on Docsity!

. 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

  1. 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