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Physiology - Block 2 - Part 1

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davidwurbel7's version from 2015-07-06 05:50

Biosynthesis of Adenocortical Hormone

Question Answer
Conversion of cholesterol to pregnenoloneCholesterol Desmolase
Rate limiting enzyme of biosynthesis of adrenocortical hormonesCholesterol Desmolase
Converts pregnenolone to 17-hydroxypregnenolone and progesterone to 17-hydropregesterone17α-Hydroxylase
Converts 17-hydroxypregnenolone to dehydroepiandrosterone and 17-hydropregesterone to androstenedione17, 20 Lyase
Converts pregnenolone to progesterone and 17-hydropregesterone to 17-hydropregesterone3β-Hydroxysteriod Dehydrogenase
Coverts progesterone to 11-deoxycorticosterone and 17-hydropregesterone to 11-deoxycortisol21β-Hydroxylase
Converts 11-deoxycorticosterone to corticosterone and 11-deoxycortisol to cortisol11β-Hydroxylase
Converts corticosterone to aldosteroneAldosterone Synthase
Aldosterone synthase is positively regulated byAngiotensin II
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Adrenal Cortex

Question Answer
Hormone that can act like Aldosterone as it is a weak glucocorticoidCorticosterone
Congenital deficiency of these enzymes leads to deficient Cortisol secretion leading to congenital adrenal hyperplasia (CAH)21 & 11 β –Hydroxylase
The most common cause of CAH is deficiency of this enzyme21 β hydroxylase
Due to absence of negative feedback inhibition in CAH, ACTH levels are elevated causingCongenital Hyperplasia of Adrenals
Congenital Adrenal Hyperplasia (CAH) is due to absence of thisNegative Feedback
Precursor steroids are increased, which get converted to androgens which leads toCongenital Virilizing Adrenal Hyperplasia
21 β hydroxylase deficiency or 11 β hydroxylase deficiency can lead to this conditionFemale Pseudohemaphroditism
Female has ambiguous genitalia at birth (classic virilizing adrenal hyperplasia); genital anomalies range from complete fusion of the labioscrotal folds and a clitoromegaly, partial fusion of the labioscrotal folds, or bothSevere CAH
This is due to due to deficiencies of 21-hydroxylase, 11-beta-hydroxylase, or 3-beta-hydroxysteroid dehydrogenaseSevere CAH
Female identified later in childhood because of precocious pubic hair, clitoromegaly, or both, often accompanied by accelerated growth and skeletal maturationMild 21-Hydroxylase Deficiency
Female may present in adolescence or adulthood with oligomenorrhea, hirsutism, and/or infertilityStill Milder 21-Hydroxylase Deficiency
Males present later in childhood with early development of pubic hair, enlargement of penis, or both, accompanied by accelerated linear growth and advancement of skeletal maturationMild 21-Hydroxylase Deficiency
Males generally have ambiguous genitalia or female genitalia; they may be raised as girls and seek medical attention later in life because of hypertension or a lack of breast development17α -Hydroxylase Deficiency
Female appear phenotypically female at birth but do not develop breasts or menstruate in adolescence; they may present with hypertension17α -Hydroxylase Deficiency
Hyperkalemia, hyponaturnia, hypovolemia and metabolic acidosis21 β hydroxylase
Hypokalemia, hypernaturnia, hypervolemia, hypertension and metabolic alkalosis11 β hydroxylase
17 α hydroxylase deficiency can lead to this conditionMale Pseudohemaphroditism
Female without secondary sexual characteristics and primary amenorrhea17 α Hydroxylase Deficiency
Male born with normal genitals. Present at age 1-4 weeks with failure to thrive, recurrent vomiting, dehydration, hypotension, hyponatremia, hyperkalemia, and shock21 β Hydroxylase Deficiency
Females at birth appear normal. At puberty, lack of pubic & axillary hair (Adrenal Androgen function) in women. Hypoglycemia (because of decreased Glucocorticoids), Metabolic alkalosis, Hypokalemia, Hypertension17α -Hydroxylase Deficiency
Males with this deficiency generally have ambiguous genitalia or female genitalia at birth; they may be raised as girls and seek medical attention later in life because of hypertension or a lack of breast development17-Hydroxylase Deficiency
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Adrenal Medulla

Question Answer
Chromaffin cells 80-90% of the cells which secreteEpinephrine
Chromaffin cells 20-10% of the cells which secreteNorepinephrine
Receptor mostly excitatory, except (-) to GIT motilityα Adrenergic Receptors
Receptor cardiac muscle – Excitatory – Increases HR, contractilityβ1 Receptors
Receptor relaxation of smooth muscle – GIT, bronchioles, blood vesselsβ2 Receptors
Dilates the pupil by relaxing ciliary muscles, causing more light to enter the eyes. Increases HR, Cardiac output, Venous return - causing better perfusion of vital organsSympathetic Response (Fight or Flight)
α1 receptors are present inBlood vessels
High levels of epinephrine cause vasoconstriction due to binding of these receptorsα1 Receptors
Norepinephrine is released by all sympathetic post-ganglionic except those neurons innervating these which release AChSweat Glands
Sympathetic post-ganglionic neurons that innervate sweat glands release this neurotransmitterACh
This neurotransmitter binds to D1 receptors in the renal system causing vasodilatationDopamine
Patient has hypertension, headache, sweating, palpitations, anxiety, moist skin, blurring of vision because of pupillary dilatation, Increased body temperature – increased BMR , Hyperglycemia leading to Glycosuria, Increased urinary excretion of catacholeamines in the form of VMA (Vanillyl Mandelic acid)Pheochromocytoma
Taper the dose of exogenous glucocorticoids to prevent thisAdrenal Insufficiency
Given along with glucocorticoids to prevent peptic ulcersProton Pump Inhibitors
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Endocrine Pancreas

Question Answer
Secretes insulinBeta Cells
Secrete GlucagonAlpha Cells
Secrete Somatostatins & GastrinDelta Cells
Inhibits the release of glucagonInsulin
Inhibits the release of Insulin & GlucagonSomatostatins
Contains the signal peptide, A chain, B chain which are connected by C-peptidePreproinsulin
Contains the A chain and B chain which are connected by C-peptideProinsulin
Contains the A chain and B chain without C-peptideInsulin
This is used to monitor insulin levels in a patient receiving exogenous insulinC-Peptide
This class of drugs causes release of insulin by blocking ATP dependent K+ channelsSulfonylurea Drugs
Tolbutamide and Glyburide are examples of this class of drugsSulfonylurea Drugs
Receptor is composed of two α subunits and two β subunits connected to each other by disulfide bondsInsulin Receptor
The β subunits of Insulin have the second messengerTyrosine Kinase
Binds to the surface insulin receptor and is phosphorylatedInsulin Receptor Substrate (IRS)
Insulin binding also causes the activation of this enzyme in addition to tyrosine kinaseProtein Phosphatase
Skeletal muscle that requires insulin to uptake glucoseResting Skeletal Muscle
Skeletal muscle that does not require insulin for uptake of glucose as excerise inducing the upregulation of GLUT 4 transporters enabling import of glucose into the muscleContracting Skeletal Muscle
Partly responsible for the decreased insulin sensitivity of target tissues in obesity and type II diabetes mellitusDown-Regulation of Insulin Receptors
Hormone responsible for decrease blood glucose concentration by Increases uptake of glucose into target cells such as muscle and adipose tissue; Promotes formation of glycogen from glucose in muscles & liver (enhances Glucokinase & Glycogen synthetase enzymes), inhibits glycogenolysis; Decreases gluconeogenesis, increases Phosphofructokinase activityInsulin
Nervous tissue, kidney tubules, intestinal mucosa, RBCs, β-cells of Pancreas are not dependent on this hormone for uptake of glucoseInsulin
Kidney tubules, intestinal mucosa and β-cells of Pancreas have this GLUT transporterGLUT 2
Nervous tissue and RBC have this GLUT transporterGLUT 1
The effect of insulin on adipose tissue activate this enzyme which breaks down VLDL and chylomicronLipoprotein Lipase
Lipoprotein lipase promotes the formation of TAGsLipogenesis
The effect of insulin on the liver inhibits this enzyme preventing lipolysisHormone-Sensitive Lipase
Inhibition of hormone-sensitive lipase decreases this actionLipolysis
On a balanced diet, Insulin: Glucagon Molar ratio is2.3
Arginine infusion increases the ratio to about3
Starvation for about 3 days the ratio is0.4
Hyperglycemic, Lipolytic, Ketogenic & Protein catabolicGlucagon
A fasting plasma glucose (FPG) level of greater than 125 mg/dL (7.0 mmol/L)Diabetes Mellitus
A 2-hour plasma glucose level of 200 mg/dL (11.1 mmol/L) or higher during a 75-g oral glucose tolerance test (OGTT)Diabetes Mellitus
A random plasma glucose of 200 mg/dL (11.1 mmol/L) or higher in a patient with classic symptoms of hyperglycemia or hyperglycemic crisisDiabetes Mellitus
Hemoglobin A1c (HbA1c) level of 6.5% or higherDiabetes Mellitus
Located in ventromedial hypothalamus inhibits feeding centre (which is located in Lateral Hypothalamus). So person stops eating & gets feeling of fullnessSatiety Centre
Satiety centre is stimulated byInsulin
Rapid, deep respirationsKussmaul Respiration
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Reproductive Physiology

Question Answer
Sex is based on sex chromosomesGenetic Sex
Sex based on histological examination of the gonadsGonadal Sex
Sex based on observation of genitalsGenital sex
Sex determining region, on the Y chromosome of genetic male fetus is responsible for development of bipotential gonad into testesSRY
Development of male type external genitalia requires hormoneDihydrotestosterone (DHT)
Testosterone is converted to Dihydrotestosterone by this enzyme5-alpha Reductase
Failure of fetal testes to secrete testosterone and Anti-Mullerian hormoneFemale external genitalia and female internal genitalia
Failure of fetal testes to secrete testosteroneFemale external genitalia and no internal genitalia of either type
Has 46 XY and functioning testes (intra-abdominal). Has male internal genitalia. Able to produce testosterone in-utero. Vagina ends as a blind pouch because there is no female internal genitalia, absent uterus & cervix. Individual is brought up as the girl till puberty. Presents with Amenorrhea5-alpha Reductase Deficiency Syndrome
Person is genetic male, has testes as gonads which secrete Testosterone and normal conversion to dihydrotestosterone (DHT). Male internal & external genitalia cannot be formed. Since AMH is present, Mullerian duct also regresses & Female internal genitalia also cannot be formed. Fetus is born with no internal gentialia and female external gentitalia.Androgen Insensitivity Syndrome (AIS)/Testicular Feminization
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Male Reproductive Physiology

Question Answer
Nourishes the developing spermatozoaSertoli Cells
LH stimulates these to secrete testosteroneLeydig cells
FSH stimulates these to produce sperm and to secrete InhibinSertoli cells
Provides negative feedback to the anterior pituitary for FSHInhibin
Provides negative feedback inhibition of LH in the anterior pituitaryTestosterone
Protein secreted from Sertoli cells to concentrate testosterone in tubulesAndrogen Binding Protein (ABP)
Cholesterol desmolase enzyme is stimulated byLH
5α-reductase inhibitor is used to treat Benign Prostatic HypertrophyFinasteride
Required for formation of internal male genitial structuresTestosterone
Required for formation of external male genitial structuresDihydrotestosterone
Has 46 XY and functioning testes (intra-abdominal). Has male internal genitalia. Able to produce testosterone in-utero. Vagina ends as a blind pouch because there is no female internal genitalia, absent uterus & cervix. Individual is brought up as the girl till puberty. Presents with Amenorrhea5-alpha Reductase Deficiency Syndrome
Person is genetic male, has testes as gonads which secrete Testosterone and normal conversion to dihydrotestosterone (DHT). Male internal & external genitalia cannot be formed. Since AMH is present, Mullerian duct also regresses & Female internal genitalia also cannot be formed. Fetus is born with no internal gentialia and female external gentitalia.Androgen Insensitivity Syndrome (AIS)/Testicular Feminization
Lower Testosterone; Increase LH; Increase FSH; Increase GnRHPrimary Hypogonadism
Lower Testosterone; Lower LH; Lower FSH; Increase GnRHSecondary Hypogonadism
Lower Testosterone; Lower LH; Lower FSH; Lower GnRHTertiary Hypogonadism
Lower Blood Testosterone; Lower Intratesticular Testosterone; Increase LH; Increase FSH; Increase GnRHOld Age
High Blood Testosterone; Lower Intratesticular Testosterone; Lower LH; Normal FSH; Lower GnRHAnabolic Steroid therapy
Normal Blood Testosterone; Normal Intratesticular Testosterone; Normal LH; Lower FSH; Normal GnRHInhibin Infusion
Lower Blood Testosterone; Lower Intratesticular Testosterone; Lower LH; Lower FSH; High GnRHGnRH Infusion (Constant)
High Blood Testosterone; High Intratesticular Testosterone; High LH; High FSH; Normal/High GnRHGnRH Infusion (Pulsatile)
Delayed puberty. Failure to develop male secondary sex characteristics. Decreased muscle mass. High pitched voice. Decreased body hair. Underdeveloped genitalia and testes. Excessive arm and leg length in relation to trunk. Tall stature. GynaecomastiaMale Hypogonadism (Before Puberty)
Erectile dysfunction (impotence). Low sperm count (infertility). Decrease in beard and body hair. Decrease in muscle mass. Increase in body fat. Decrease in size of testes. Gynecomastia. Loss of bone mass (osteoporosis). Decreased libido. Fatigue and anemia. Emotional instabilityMale Hypogonadism (After Puberty)
Persistent inability of a couple to have a child due to certain problems in the male partnerMale Infertility
Defective spermatozoa or defective spermatogenesis are reasons forMale Infertility
Removal of testes. Clinical picture is same as that of hypogonadism before or after pubertyCastration
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