endocrine system notes pdf

Endocrine System notes

👉Ductless glands -Products of endocrine glands circulate in blood directly without ducts.

Hypothalamus :- Situated in the cerebrum, below the thalamus.

Releases GHRH & GHRIH 
  • Inhibit growth.
  • Inhibit Insulin & Glucagon.

👉Hypothalamus hormone :


(1) Corticotropin releasing hormone (CRH).

(2) Gonadotropin releasing hormone (GnRH).

(3) Growth hormone releasing hormone (GHRH).

(4) Thyrotropin releasing hormone (TRH).

(5) Growth hormone inhibiting hormone (GHIH). (Somatostatine)  (Imp. Q )
  • Inhibit growth.
  • Inhibit Insulin & Glucagon.
(6) Melanocyte releasing hormone (MRH).

(7) Prolactin releasing hormone (PRH).


Largest endocrine gland :- Thyroid (Imp. Q )
Largest exocrine gland- Liver (Imp. Q )

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Pituitary (Hypophyseal) Gland


1. Pituitary (Hypophyseal) Gland.
  • Master gland Hypothalamus → Control pituitary gland
  • Pea shape
  • note- (Split pea shape - Parathyroid gland).
  • Weight :- 500 mg
  • Located in sella turcica cavity of sphenoid bone.
👉Lobes are :

Anterior pituitary Lobe
  • Adenohypophysis- Connected by blood vessels with Hypothalamus.
Posterior pituitary Lobe
  • Neurohypophysis- Connected by nerve c̅ Hypothalamus.
  • (Both Lobes are :- Connected by Intermediate lobe.)
Hormones released by pituitary gland are :

👉Anterior gland Hormone :

(1) Growth hormone

(2) TSH (Thyroid Stimulating Hormone)

(3) ACTH (Adrenocorticotropic Hormone)

(4) FSH

(5) LH

(6) Prolactine

(7) MSH ( Melanocyte-stimulating hormone )

👉Posterior gland Hormone :

(1) Oxytocin

(2) Vasopressin (ADH) (Antidiuretic hormone.)

Synthesize in hypothalamus & Storage in posterior Pituitary & Released by Posterior pituitary.

(1) Growth hormone :

a) Increased

I. Gigantism :- Before bone epiphyseal closure Occurs in child (Whole body enlarge )

II. Acromegaly. :- After bone epiphyseal closure In adult ( Extremities enlarged )
Somatostatin Replace

b) Decreased

I. Dwarfism

II. Growth retardation (Shunting) to switch Growth hormone replaced


(2) TSH (Thyroid Stimulating Hormone):- It is controlled by Thyrotropin-releasing hormone TRH → From hypothalamus
   ↓
Stimulate thyroid gland to release
  ↓
T3 (Tri-iodo thyronine) and T4 (Thyroxine)

Q.: The Impact of ↑ed T3 & T4 on TSH is

Ans. ↓TSH, Rationale : (By negative feedback)
 

(3) ACTH ( Adrenocorticotropic hormone ) - It is regulated by ACTRH (From hypothalamus)
                       ↓
It has control over Adrenal Gland

(4) FSH - Follicle stimulating hormone. It Matures ovarian follicles in the ovarian cortex. Growing follicles releases estrogen

Estrogen ↑ then FSH ↓se & LH ↑es.

(5) LH-Luteinizing hormone.
  • Function :- Rupture of Graffian follicle.
  • Maintenance of corpus luteum.
  • Progesterone ↓ then LH ↓es & FSH ↑es.

(6) Prolactin :- Production/Synthesis of milk.
  • For breast alveoli functioning & maturation
  • Natural contraception due to prolactin hormone.
  • It inhibits estrogen & progesterone.
  • Anovulatory menses occurs during EBF.
Homeostasis :- State of Equilibrium. 
-Ve Feedback Mainly maintained
like this ↓TSH, Rationale : (By negative feedback)

↑ = ↓

↓ = ↑

+ Feedback like this

↓ = ↓

↑ = ↑

Eg-Labour Contraction ↑ , Oxytocin ↑ .


Posterior Pituitary -

(1) Milk ejection hormone - Oxytocin
Milk releasing hormone - Oxytocin
(note- Prolactin :- Production/Synthesis of milk. )

(2) Vasopressin (ADH).

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👉ADH Decreased
  • DI (Diabetes insipidus)
  • ADH↓= Urinary output ↑se (Polyuria=5-25 L/day)
  • Increased Thirst → Polydipsia.
  • Treatment :- Give ADH.
👉ADH Increased
  • SIADH (Syndrome of Inappropriate ADH).
  • ADH↑ = Urinary output ↓se.
  • Blood volume ↑se.
  • Electrolyte imbalance.
  • Hyponatremia
  • Water intoxication (Due to increased fluid or water loss dehydration may occur. )

it may cause loss of body weight.
  • If 5% body weight loss →Mild dehydration
  • 5-10% body weight loss = Moderate dehydration
  • > 10% body weight loss → Severe dehydration
👉 In DM :- Polyuria, Polydipsia, Polyphagia + weight loss (cachexia=weakness in body)

👉ADH:- Act on nephron tubules to reabsorb H2O.
S/S :-
  • Polyuria 5 to 24 L/day (Most Indicative)
  • Polydipsia :-increased thirst due to Dehydration
  • Urine specific gravity (1.006 or lower)
  • Postural hypotension :- Tachycardia.

Intervention :

(1) Safe environment

(2) Avoid food or liquid that produce diuresis.

👉Sever DI
  • Give vasopressin tannate IM/Orally.
  • Give desmopressin acetate (DDAVP).
  • SIADH  (Syndrome of Inappropriate ADH )
  • Excess ADH released without body needs.
  • Results in water intoxication & hyponatremia.
  • S/S:- Wt gain, HTN, Tachycardia, Fluid overload; change in level of consciousness.
Intervention :

(1) Safe environment. (2) Restrict fluid Intake.

(3) Give diuretics & I.V. fluid (NS or hypertonic saline).


Pan-hypo-pituitarism :- Decrease all hormones of pituitary gland

Simmond's Syndrome /Sheehan's syndrome.

Hypo-physe-ctomy :- (Pituitary adenectomy, transsphenoidal)

Pituitary surgery (Endoscopic trans-nasal) -
  • Removal of pituitary tumour via craniotomy or trans-Sphenoidal approach.
Postoperative care :

(1) Elevate the head of the bed.

(2) instruct client to avoid sneezing, coughing, blowing of the nose (to prevent ↑ICP).

(3) Monitor for Diabetes insipidus or SIADH.

(4) Avoid water intoxication.

(5) Administer glucocorticoids

(6) After transsphenoidal hypophysectomy-Check nasal discharge for glucose presence of glucose in nasal if discharges indicate leakage of CSF.
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Thyroid Gland

Largest endocrine gland. SIZE- 5 x3 x2 cm
(note- Largest gland liver )

Anatomical location : C-5, C-6, C-7

WEIGHT: -30 gm ,Two lobes, Connected by Isthmus

Lobes are made of Lobules, Lobules are made of Acini that Releases thyroid hormone (T3 &T4) 

T3 -0.5 ug/dl & T4 - 0.8 ug/dl
 
Parafollicular cells (C - cells)- these are between the follicles of thyroid gland. 
C-cells release Calcitonin

Function of calcitonin are - Decrease Serum calcium By
  1. Bone mineralization ↑se
  2. Intestinal absorption ↓se
Calcitonin↑ Hypocalcemia (↓Serum calcium level) → Tetany

Chvostek Sign → Facial spasm

Trousseau's Sign → Carpal spasm.

Management :

Calcium gluconate -10meq /10ml/ 10minute

↓Calcitonin :- Hypercalcemia -Cause urolithiasis.


Q.: In case of ↓Calcitonin which disorder may оссur. 

(1) Cholelithiasis → ↑es cholesterol

(2) Urolithiasis. (Calcium oxalate - most common stone in kidney.)

(3) Tetany due to increased calcitonin

(4) All of above
 
ANSWER: 2
(Calcium oxalate - most common stone in kidney.)
Function of thyroid gland :
  1. Metabolism
  2. Growth & Development
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Thyroid hormone

A) ↑(Hyper-thyroidism)

(1) Grave's disease (toxic diffuse goiter )

• Metabolic rate ↑es.

• Weight loss, temperature ↑  Dry skin

• Heat Intolerance, Diarrhoea, Tachycardia

• Exophthalmos

• Eye protrusion (classical sign)

Anti-thyroid drug- to ↓ T4 & T3

* Drug of choice.- PTU (Propyl-thio-uracil). (Imp. Q )

- Potassium Iodide.

- Radioactive iodine (I131) (Imp. Q )
          ↓
Damage tumour cells.

PTU Side effect = Agranulocytosis. (WBC) (Imp. Q )


B) ↓(Hypothyroidism)

(1) Cretinism :- In child

(2) Myxedema :- In adult

(3) Goiter :- Autoimmune Goiter

Endemic Goiter- due to iodine deficiency

• Cold Intolerance

• Weight gain

• Temp ↓es, ↓appetite

• Constipation

• Moist skin, Bradycardia

Treatment

Thyroid replacement

Levothyroxine sodium(Drug of choice)(Imp. Q )

Cardiac Stimulant = ↑HR

👉 Environment in Hyperthyroidism :- Cool environment

👉 Environment in Hypothyroidism :-Hot environment

👉 Diet in Hyperthyroidism :- High calorie

👉 Diet in Hypothyroidism :- Low calorie


Q: Levothyroxine Sodium may cause (Imp. Q )

Ans: ↑Heart rate.

Nurse action → Monitor vital signs, specifically Heart rate.


Goiter :- Enlargement of thyroid gland & T3& T4 ↓se.

Autoimmune Goiter (Hashimoto's disease)

Endemic Goiter (Iodine deficiency goiter)
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Myxedema coma - Serious hypothyroidism.

c/s
  1. Hypotension
  2. Hypothermia
  3. Hyponatremia
  4. Bradycardia
  5. Respiratory failure.
  6. Coma.
👉Thyroid Storm :- Uncontrolled hyperthyroidism.

↑ed temperature, tachycardia. Systolic HTN, Delirium, coma

Do Not give salicylates (They ↑free thyroid hormone level.)(Imp. Q )

treatment :-
  1.  Glucose I.V
  2. Levothyroxine Sodium.
  3. I.V. fluid.
  4. Patient airway maintains
Thyroidectomy :- Removal of thyroid gland.

Preoperative :

(1) Check vital signs, weight, electrolyte level.

(2) Assess for hyper-glycemia.

(3) Check for thyroid storm & give medicine.

Post operative :

(1) Monitor for respiratory distress.

(2) Have a tracheostomy set, O2 & suction at bedside.(Imp. Q )

(3) Limit talking, assess level of hoarseness.

(4) If parathyroid damage-Assess for hypocalcemia & tetany.

(5) For tetany-Give calcium gluconate.

(6) Give a semi fowler position.(Imp. Q )


Endocrine /Metabolic disorder of pancreas

DIABETES MELLITUS (Imp. Q )

Symbol for DM is Blue circle 

> Normal Glucose:- 70-110 mg/dl

Prediabetic :- 100-125 mg/dl

Diabetic :-> 126 mg/dl (Fasting level)

DM -Mechanism of onset of clinical features :

decrease Insulin
        ↓
↑serum glucose level
       ↓
Osmolarity ↑
Transport of fluid into blood vessels.
       ↓
GFR ↑se
       ↓
Polyuria (Imp. Q )
Baroreceptor Stimulation
       ↓
Thirst centre stimulate
       ↓
Thirst↑ (Polydipsia) (Imp. Q )
       ↓
Appetite increases : Polyphagia (Imp. Q )


Secondary DM.

(1) (Cushing syndrome)
  • ↑Gluconeogenesis
  • ↑ Glucocorticoids
(2) Steroid therapy.


Types of DM

I. IDDM (Type 1)

Juvenile DM Non functioning of beta cells

Exogenous Insulin is effective to treat type IDM

Complications are: DKA (Diabetes ketoacidosis) (Imp. Q )

II. NIDDM (Type II)

Maturity onset Diabetes

Increases Resistance of Cells to insulin.

Obesity is a common cause

Oral hypoglycemic/Antidiabetic drug given to treat type II DM.

HHNDKA - Hyperglycemic hyperosmolar Non diabetic ketoacidosis (Imp. Q )

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Investigations:

Fingertip method :- Reliable method to diagnose DM.: Punctare lateral side, not midpoint bcoz nerve + nt

OGTT :- Oral glucose tolerance test - Confirmatory test 75gm sugar add in 300ml of H20. (Range 50– 200gm).

Sample after 2 hour = PP Sample > 200mg/dl 👉DM.

Post prandial sugar: (2 hour after eating)

RBS (Random blood sugar)

Normal - < 200 mg/dl

Diabetic -> 200 mg/dl. (At last on 2 occasions.)

Glycosylated Hb - blood glucose bound to Hb.

HbA1C =Glycosylated HbA1C indicate increased glucose from past 3-4 month. (Imp. Q )
  • Normal Value HbA1C -(4-6 %)
  •  In DM Value HbA1C -  (7%) & more
In this test fasting is not required.

DKA.(Diabetic ketoacidosis):

Mechanism :
↑ Blood Glucose
       ↓
 ↓es cellular glucose level
       ↓
Starvation in cells
       ↓
More eating (Polyphagia)
       ↓
More sugar level ↑es in blood & cellular level is deprecated
       ↓
Starvation in cells
       ↓
Body weight↓ (Cachexia); 
Fat metabolism occurs
        ↓
 Ketone bodies form
      ↓
Kaussmal's respiration (Regular, deep & rapid)
( 3P + Weight loss + Kaussmal breathing
P-Polyuria
P -Polydipsia
P-Polyphagia
  • DKA :-Glucose => 250-300 mg/dl.
  • PH = < 7.35 (Acidic)
  • Bicarbonate = < 15 meq/1
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Clinical features :
  • Fruity breath odour. (Sweet)
  • Ketonuria (Rothera's test)
  • Dehydration.
Diabetic coma Due to excess ketone in blood.

In DKA:
  • Ketosis & acidosis occurs & K+ level ↑es, 
  • (Priority:Rehydration is done c̅ I. V. Infusion of NS 0.9% or 0.45%),
  • then serum K+ level ↓es & need K+ replacement.
  • After this < 240 mg/dl then give I.V. fluid c̅ 5% dextrose.
  • Use regular Insulin only to treat DKA.(5 to 10 uint)
  • In DKA glucose level (> 250 mg/dl)
  • In DKA PH (< 7.35)
  • In DKA Plasma bicarbonate (< 15 meq/L)
  • Urine Ketone +nt.
C/M

Kaussmaul's respiration, fruity breath odour, nausea, abdominal pain-Due to ketosis.
Polyuria, Polydipsia, weight loss, dry skin, blurred vision,
lethargy, coma-Due to dehydration.

Hyperglycemic hyperosmolar nonketotic syndrome (IIHNS)- In type II DM.

Extreme hyperglycemia without ketosis & acidosis

Rehydration (NS) alone may decrise glucose level

C/M
  • Altered CNS function c̅ neurologic symptoms.
  • Other than DKA.
  • Serum Glucose = > 800 mg/dl.
  • PH= > 7.4
  • HCO3 = > 20 meq/L.
  • Ketone = Negative.
Gestational DM =
  • Newborn of a diabetic mother :- Macrosomic, Hypoglycemic.
Management:

Type I :- Insulin therapy. Route: SC-45° or IV infusion

Type II :- Sulfonylurea-Choice of drug.
  • Oral antidiabetic/Hypoglycemic drugs.
Chronic Complication of DM:

(1) Diabetic retinopathy :- Impaired retinal circulation & hemorrhage.

Early T/t - Control HTN & blood glucose level.

(2) Diabetic Neuropathy :
  • Complication-Non healing ulcer of foot, gastroparesis, erectile dysfunction.
  • Mostly damage to IV & VI cranial nerves.
  • Cause orthostatic hypotension.
  • Skin breakdown, sign of infection (Check for ↑ed temp)
  • Foot care is needed - Never remain barefoot.

(3) cardiovascular & peripheral vascular disease 

Acute complication

(1) Hypoglycemia

(2) DKA

(3) Hyperosmolar hyperglycemic state.
Types of Insulin


Activity Profiles of Different Types of Insulin


1. Immediate acting :- Lispro, 
  • Contraindicated in Pregnancy induced DM (Gestational DM) 
  • Onset of action :- 5-15 minutes

II. Short acting
  • Semilentle (Regular)
  • Onset of action: 30 minutes
III. Intermediate acting
  • Lente
  • NPH
  • Onset of action: 60 minutes
IV. Long acting

Ultralente 
  • Best Combination : - Regular Insulin + NPH
  • syringe; Iml = 40 unit
  • I unit - 0.25ml
  • Store in Refrigerator
  • Open vial used for: 28 day

Injection site :- Arm, thigh, Abdomen, buttocks

Forearm most common site in adult

In periumbilical region: 1 inch away from umbilicus

Lipo-hyper-trophy Elevation of tissue at injection site; So administer Insulin at different site in rotatory manner.

Lipo_atrophy / Lipo_dystrophy > Irritation & damage of SC tissue & fat


Complication of Insulin therapy :

(1) Redness, swelling, tenderness at site of Injection.
* Clean the skin with alcohol before injection.

(2) Insulin lipoatrophy-loss of SC fat & slight dimpling or pitting at the injection site.

Lipo-hyper-trophy-Develop fibrous fatty masses at Injection site.

So rotate Injection site.

(3) Dawn phenomenon

Hyperglycemia (5 to 8 AM.) → Pre Breakfast, caused by nocturnal release of GH.

Tlt - Evening dose of Intermediate acting Insulin at about 10 PM is Increased.

(4) Somogyi phenomenon

Elevated blood glucose level at bedtime, hypoglycemia at 2-3 AM,

counter regulatory hormone acts & at 7AM, hyperglycemic occurs.

Tlt - Evening dose of Intermediate acting Insulin is decreased

(5) Insulin resistance-Body cells not responsive to Insuline 

(6) hypoglycemia
  • Mild hypoglycemia - Blood sugar< 60 mg/dl
  • Moderate hypoglycemia - < 40 mg/dl 
  • Severe hypoglycemia - < 20 mg/dl
C/M- Confusion, diaphoresis, Tremors, Irritability, Nervousness, Slurred speech, Palpitation

In unconscious or semi conscious people - Not giving oral food having severe hypoglycemic bcoz risk for aspiration 
Give IM. or S/C. glucagon or In hospital 25-50 ml of 50% dextrose (IV)


In DKA Notify physician when : Vomiting, diarrhoea, fever persists.

Glucose - 250-300mg/dl. 

Adrenal Gland

  • Superior border of Kidney.
  • Retroperitoneal
  • size- 3 x 2 x 1 cm, Weight = 5 gm
Parts of adrenal gland

1. Cortex - Hormones released are
  •  Glucocorticoid (Cortisol/Steroid)
  • Mineralocorticoid (Aldosterone)
  • Some Adnrogen (Sex/Gonadal hormone
2. Medulla :- Epinephrine & Nor- Epinephrine,

Pheochromocytoma :- Tumour of Adrenal medulla. Benign tumour

Increase Secretion of catecholamines (Increase Epinephrine & nor-epinephrine)

Metabolism of catecholamines forms VMA (Vanillylmandelic acid)

VMA test: For confirmation of Pheochromocytoma 24 hour urine sampling needed (Imp. Q )

> 10mg = Indicate pheochromocytoma


Glucocorticoids :- Gluconeogenesis ( ↑blood glucose level)
  • Immunosuppressant
  • Glycogenolysis.
  • Delay wound healing

Aldosterone :- Fluid & Electrolyte balance.

Androgen :- Growth of genitals.

(1) Cushing syndrome → ↑ed glucocorticoids

Clinical features :- Moon face, buffalo hump (fat deposition) Hyperglycemia, ↓ed Immunity

Electrolyte imbalance.

(2) Conn's Syndrome :- Hyper_aldosteronism.

-Fluid & electrolyte imbalance.
  1.  ↑es water + Sodium retention. (Hypernatremia)
  2. ↓es potassium (Hypokalemia)
  3. Hypertension.
ECG Change :-U-wave appear, T-flat - Hypokalemia (Imp. Q )

(T wave elevated, QRS wide - Hyperkalemia(Imp. Q )

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Fluid & electrolyte balance through Renin Angiotensin- Aldosterone Axis

Angiotensinogen (Liver) 
        ↓- Renin(by Kidney)
 Angiotensin I
      ↓ ACE (Lungs)
Angiotensin II
    ↓
Aldosterone.
     ↓
Sodium & water reabsorption & Vaso- constriction

Q. A patient is on steroid therapy with Investigation is most Important

(1) Urea breath test

(2) Uric acid test

(3) Serum glucose test 

(4) VMA test

ANSWER: 3
  • Urea breath test is for H. pylori 
  • VMA (Normal 4-6 ng/dl, more than 10 abnormal) 
  • test is for Pheochromocytoma. 
  • serum Uric acid for renal failure
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Addison's disease :- most common symptoms hyper pigmentation of skin (albright syndrome)
  1. Hypoglycemia
  2. Hypotension
  3. Hyponatremia
  4. Hyperkalemia.
Drug :- Steroid therapy
Steroids may be :

Long acting :- Dexamethasone-Drug given in → Tapered fashion

Intermediate acting :- Prednisolone

Short acting :- Hydrocortisone

Adrenal gland disorder :

Function of glucocorticoids :- Gluconeogenesis, Anti inflammatory, Immunosuppressant

Function of mineralocorticoids:- Na & H2O reabsorption. (Aldosterone)

In both check B.P., Glucose & Electrolyte level

Addison's Disease

Hyposecretion of cortex hormone (Glucocorticoid, Mineralocorticoid)

S/S
  1. Weight loss
  2. Hypoglycemia
  3. Hyponatremia
  4. Hyperkalemia, hypercalcemia
  5. Postural hypotension
  6. Hyperpigmentation of skin.
  7. GI disturbances.
  8. Lethargy, fatigue, muscle weakness.

Cushing's disease/Syndrome - Hyper-cortisolism.

Hypersecretion of glucocorticoids from cortex.
S/S
  1. Weight gain.
  2. Hypernatremia.
  3. Hypokalemia, hypocalcemia.
  4. HTN
  5. Truncal obesity, c̅ thin extremities,
  6. Moon-face.
  7. Buffalo hump.
  8. Muscle wasting & weakness
  9. Fragile skin.
  10. Labile mood, Psychosis, Euphoria.
Provide meticulous skin care, 
Hypophysectomy (When ↑ACTH is a cause) 
Adrenalectomy

Diet
  1. High protein & high carbohydrate & Normal Na+
  2. Need for life long glucocorticoid therapy.(Imp. Q )

Addisonian Crisis

Hyposecretion of adrenal gland.
Life threatening disorder caused by acute adrenal insufficiency
Precipitate by stress, Infection, trauma, Surgery

C/S
  1. Severe headache, severe abdominal, leg, lower back pain.
  2. Weakness, Irritability & Confusion.
  3. Severe hypotension, Shock.
treatment
Initially give- Hydrocortisone sodium succinate. 

Conn's Syndrome. (Hyperaldosteronism) ↑aldosterone.
Cause-Adenoma (Imp. Q )

S/S
  1. Hypokalemia Hypernatremia, HTN
  2. Polydipsia & Polyuria.
  3. Specific gravity of urine is low
  4. Metabolic alkalosis.
treatment
  • Spironolactone (K+ Sparing diuretic)
  • Adrenalectomy. (Give corticosteroid postoperatively)
Pheochromocytoma:-Tumour of Adrenal medulla.(Imp. Q )

* HTN is hallmark (Imp. Q )
  • Catecholamine-producing tumor
  • Benign tumour.
  • Excessive epinephrine & norepinephrine secreted.
S/S
  1. HTN, Hyperglycemia, Diaphoresis.
  2. Pain in chest & abdomen c̅ nausea & vomiting
  3. Weight loss. - Heat Intolerance
  4. Dysrhythmia. - Heart beat ↑es & Irregular
Diagnostic test :
  • Vanillyl mandelic acid (VMA)-24 hour urine collection - Check for VMA
  • (Normal - 10 mcg/100ml) - ↑ed in pheochromocytoma.
  • Avoid, Abdominal pressure, Vigorous abdominal palpation

treatment
  1. Adrenal gland removal.
  2. Give rest & non stressful environment & avoid stimuli.
  3. Monitor for hypertensive crisis.
Diet

* High calories, vitamins & minerals.

Adrenalectomy :

Lifelong gluco & mineralocorticoid is necessary

Catecholamines drop, check for cardiovascular collapse, hypotension, shock.

Hemorrhage may occur - Adrenal gland is highly vascular

Preoperative :

(1) Monitor for hyperglycemia, electrolyte level & prevent infection.

Postoperative :

(1) If Urine output < 30 ml/hr, notify physician, (renal failure, shock may occur).(Imp. Q )

(2) Monitor for hemorrhage (24 - 48 hour) 

(3) Paralytic Ileus-Sign-Abdominal distension, pain, nausea, vomiting, ↓ed bowel sound. Occur due to internal bleeding, anesthesia effect.

(4) Prevent atelectasis.

4. Parathyroid Gland

Split pea shape, 4 Lobe

↑ Activity of Osteoclast cells, Serum calcium increases, Serum phosphate ↓es

Parathyroid works Opposite to Calcitonin

Parathyroid ↑es -Hypercalcemia(increase Serum Ca.) (Urolithiasis)

Parathyroid ↓es - ↓ Serum Calcium ↑ Phosphate

(Imp. Q ) Decrease calcium in blood Causes Tetany- It is manifested by Spasm of larynx
  • Chovestik sing (facial spasm)
  • Trousseau's sign (carpal spasm)

Treatment :- Calcium gluconate
  • 10    :  10   : 10
  • Meq : ml   : nin
In case of ↑ phosphate give Aluminium

Hydroxide = ↓es adsorption of phosphate from GIT.

Milk, cheese, dairy products are not given in hypoparathyroidism.

Because it increases serum phosphate.

Hypo-parathyroidism :- ↓ed parathormone.

C/M

Hypo-calcemia & hyper-phosphatemia.

Numbness & tingling in face.

+ ve Trousseau's sign & Chvostek's sign (Tapping on facial nerve](Imp. Q )

Hypotension, bronchospasm, laryngospasm, dysphagia.

Intervention :

(1) Place tracheostomy set, O2, Suction catheter at bedside.(Imp. Q )

(2) Give calcium gluconate.

(3) Give a high calcium, low phosphorus diet.

(4) Give vitamine D.

(5) Give phosphate binders to excrete phosphate.

Hyperparathyroidism :-↑ Parathormone.

Anorexia, Nausea, Vomiting, Constipation

Hypercalcemia & hypophosphatemia Weight loss

Hypertension, Cardiac dysrhythmias, Renal stone.

Intervention :

(1) Monitor B.P.

(2) Give furosemide-To lower ca+

Parathyroidectomy: - Removal of one or more parathyroid glands.

Post operatively :

(1) Monitor for respiratory distress

(2) Tracheostomy set, O2, Suctioning at bedside.

(3) Semi fowler position.

(4) Assess neck dressing for bleeding.

(5) Monitor for hypocalcemia & tetany,

(6) Monitor for laryngeal nerve damage

(7) Give ca+ & vit D.
nursing officer app online test series link- https://tinyurl.com/yfyq5nyr?utm_source%3Dcopy-link%26utm_medium%3Dtutor-course-referral%26utm_campaign%3Dcourse-overview-app
Thymus  - Anatomical location. In the thoracic cavity.

Secretes Thymosin hormone
          ↓
Maturation of T-Lymphocyte (Imp. Q )
         ↓
Cell mediated immunity.

Pineal Gland

Anatomical location: Midbrain

Attached to Lateral ventricle.

Hormome → Melatonin


DIAGNOSTIC test
(Imp. Q )

test (1) Stimulation testing
- Stimulate gland → Normal secretion not occur → Hypofunction

test (2) Suppression testing -Suppress gland → Secretion not ↓es →Hyperfunction.

test (3) Radioactive iodine uptake-To check thyroid function.
  • Radioactive Iodine is given.
  • 2 to 4 hour after giving - 3%-10% Normal value.
  • 24 hour after given - 5 to 30%
👉 Radioactive iodine uptake Elevated - hyperthyroidism.
👉 Radioactive iodine uptake↓ed - hypothyroidism.

(4) T3 & T4 resin uptake test.

↑sed - In hyper ↓sed - In hypothyroidism,

(5) TSH level-(Normal – 0.2 to 5.4 microunit/ml).

TSH ↑sed - Hypothyroidism.

TSH ↓sed - Hyperthyroidism or secondary hypothyroidism.

(6) Thyroid scan-Identify nodules in thyroid gland.

Radioisotope of iodine or technician is administered

Test is contraindicated in pregnancy  (Imp. Q )

(7) Glucose tolerance test
- D.M. (Imp. Q )

PD (Postprandial) blood sugar > 200mg/dl- D.M. + ve.

Before 36 hour of tests, avoid alcohol, caffee, smoking (Imp. Q )

10-12 hours NPO for fasting sugar check.

After taking a fasting blood sample, a glucose drink is given & then check blood at 30 minute interval of 2 hours

(8) Glycosylated Hb - blood glucose bound to Hb.

HbA1C =Glycosylated HbA1C indicate increased glucose from past 3-4 month. (Imp. Q )
  • Normal Value HbA1C -(4-6 %)
  •  In DM Value HbA1C -  (7%) & more
In this test fasting is not required.

(9) Glycosylated serum albumin (Fructosamine) -
  • Non Diabetic - 1.5 to 2.7 mmol/L. More sensitive
  • Diabetic pt - 2 to 5 mmol/L. Than HbAIC


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