Why is venous blood more acidic than arterial blood?

State the pH of each.

What pH boundaries are life threatening? why?

Venous blood (7.35) has more pCO2 and CO2 + H2O=carbonic acid.

Arterial blood pH: 7.45

LIFE THREATENING: 6.8>pH>8.0, because all enzymes/metabolism cannot function.

EXTRACELLULAR FLUID (ECF)

1) The fluid directly bathing outside of cells

2) Fluid in the vessels/lymphatics

*State major cations/anions of ECF and ICF.

1) INTERSTITIAL: The fluid directly bathing outside of cells. 

Na+, Cl-.

2) INTRAVASCULAR/PLASMA: Fluid in the vessels/lymphatics.

Na+, Cl-, & Protein Anions (albumin).

ICF: K+, phosphate-, protein-

Water Gains/Day

1) Major Input

2) Major Output

1) Major Input: drinking (60%), water (30%), oxidation

2) Major Output: urine (60%), lungs (30%), skin (10%), stool

Plasma Protein:

1) name a Major prot player and function

2) name clotting protein

3) Net charge of proteins in blood

4) 3 causes of edema (due to protein def)

1) albumin= osmotic force that draws H2O into capillaries

2) fibrinogen: clotting protein

3) Net charge is negative (anion)

4) 3 causes of edema:

-Liver disease: no synthesis of protein

-Kidney Disease: protein excreted vs reabsorbed

-Malnurishment: Amino acids for prot synthesis not ingested

Strong Cation Gradients between ECF & ICF:

Strong (Fast Movement)

Na+ into cell

K+ out of cell

Weak (slow movement)

Ca++ into cell

Mg out of cell

Water Movement:

What happens if you place a cell in...

1) hypotonic solution

2) hypertonic solution

1) Cell swells (A hypotonic solution contains a lesser concentration of impermeable solutes than the solution on the other side of the membrane)

2) Cell shrinks (A hypertonic solution contains a greater concentration of impermeable solutes than the solution on the other side of the membrane)

State the Mechanisms of Edema from the following causes:

1) Burns, Allergic Inflamm Rxn Mech

2) Cirrhosis, Malnutrition mech

3) Venous Obstruction, Na+/H2O Retention, Heart Failure mech

4) Lymph Obstruction

1) Burns, Allergic Inflamm Rxn Mech: incr capillary permeability => lose plasma prot => incr tissue & decr capillary oncotic pressure

2) Cirrhosis, Malnutrition mech: decreased plasma prot production => decr capillary oncotic pressure

3) Venous Obstruction, Na+/H2O Retention, Heart Failure Mech: increased capillary hydrostatic pressure => fluid mov't into tissue => Na/H2O renal retention

4) Lymph Obstruction: decr absorption of interstitial fluid

Regulation of BP through Fluid Volume:

1) Na+/Cl- balance (4)

a) incr reabsorption of Na+

b) decr reabsorption of Na+

c) vasocontriction/Na+ retention

d) Where does chloride come into all this??

2) Water balace (2)

a) incr reabsorption of H2O in kidney tubules

b) controls water intake

1) Na+/Cl- balance

a) Aldosterone: steroid hormone from adrenal cortex.  acts on kidney tubules to incr reabsptn of Na+

b) ANP/BNP: peptides secreted with atrial/ventricular stretching & act on kidney to decr reabsptn of Na+.

c) RAAS: renin is enzymatic kidney protein stimulated with low bld vol/low BP/low Na+

(Renin>AngI>AngII>Ald...vasoconstriction & Na+ ret)

c) Cl- always follows Na+

2) Water balace (2)

a) Vasopressin: ADH secreted from post pituitary incr reabsorption of H2O in kidney tubules

b) Osmoreceptors in Hypothalamus control thirst.

Water/Solute Balances.  State ECF conc % of NaCl (salt):

1) Isotonic (Isoosmolar) imbalance:

2) Hypertonic (Hyperosmolar) imbalance:

3) Hypotonic (Hypoosmolar) imbalance:

1) Isotonic (Isoosmolar) imbalance: 0.9%

2) Hypertonic (Hyperosmolar) imbalance: >0.9%.  Water loss or solute gain = cells shrink.

3) Hypotonic (Hypoosmolar) imbalance: <0.9%.  Water gain or solute loss = cells swell.

Resulting Tonicity Imbalances.....

1) Hyperaldosteronsism, cushings

2) diarrhea, diabetes insipidus, excess diuresis/diaphroesis

3) Hyperglycemia

4) Excess diuretic therapy, hypoaldosteronsism

5) Overhydration

6) Nephrotic syndrome, cirrhosis, cardiac failure

Hypertonic Imbalances

1) Hypernatremia (synonymous with dehydrated, resulting in incr Na concentration): Hyperaldosteronsism, cushings

2) Water deficit: diarrhea, diabetes insipidus, excess diuresis/diaphroesis

3) Dehydration: Hyperglycemiacauses polyuria

Hypotonic Imbalances

4) Hyponatriremia: Excess diuretic therapy, hypoaldosteronsism

5) Water excess: Overhydration

6) Nephrotic syndrome, cirrhosis, cardiac failure cause edema

State the electrolyte imbalance:

1) Most common causes are hyperparathyroidism, bone metastesis, excess vit D.  Causes incr in neuromuscular excitability.

2) decr neuromuscular exitabolity & cardiac dysrhythmias

3) Assoc with cell detruction (like tumor & chemo).  *What other electrolyte imbalance can this cause?

4) Causes depression of skeletal muscle contraction and nerve function

5) related to inadequate intestinal absorption, bone formation, hypoparathyroidism, vit D deficiency. Causes decr in membrane excitability.

6) Associated with DM.

*Signs/sx similar to which other electrolyte imbalance?

7) Could be due to decr renal excretion.  ECG changes: acute T wave, wide WRS, ST depression.

8) Assoc w/ vit D def, alcoholism, malabsorption syndromes.

*When do symtoms become evident?*

State the electrolyte imbalance:

1) Hypercalcemia: Most common causes are hyperparathyroidism, bone CA metastases, excess vit D.  Causes incr in neuromuscular excitability.

2) Hypokalemia: decr neuromuscular exitability & cardiac dysrhythmias. Seen in diabetic ketoacidosis.

3) Hyperphosphatemia: Assoc with cell destruction (like tumor & chemo).  *Can cause hypocalcemia.

4) Hypermagnesemia: Causes depression of skeletal muscle contraction and nerve function

5) Hypocalcemia: related to inadequate intestinal absorption, bone formation, hypoparathyroidism, vit D deficiency. Causes decr in membrane excitability.

6) Hypomagnesemia: Associated with DM.

*Signs/sx similar to hypocalcemia.

7) Hyperkalemia: Could be due to decr renal excretion. K+ to ECF.  ECG changes: acute T wave, wide WRS, ST depression.

8) Hypophosphatemia: Assoc w/ vit D def, alcoholism, malabsorption syndromes.

*symptoms become evident with severe depletion*

Hormonal regulation of Ca balance:

How does the body reguate hypercalcemia & hypocalcemia?

Parathyroid hormone (PTH).

Hypercalcemia:

-decr PTH

-decr renal activation of vit D

-decr Ca intestine absorption/renal absorption/bone reabsorption & decr phosphate excretion.

Hypocalcemia:

-incr PTH

-incr renal activation of vit D

-incr Ca intestine absorption/renal absorption/bone reabsorption & incr phosphate excretion.

4 acid base balance mechanisms

1) pH determined by a ratio

2) instantaneous response.

3) carbonic anhydrase rxn

4)  H+ / bicarb excretion/retention

1) Henderson-Hasselback:

pH= ratio of bicarb:CO2.

7.4= 20:1.

Incr bicarb=incr pH//Incr CO2=decr pH.

Bicarb controlled by kidneys (bicarb retained or H+ excreted).

CO2 controlled by lung/RR.

2) Buffer systems: weak but instantaneous.

Bicarb, hemoglobin, phosphate, protein.

3) Respiratory Control:

carbonic anhydrase rxn...this enzyme catalyzes rapid conversion of CO2 to bicarb.  CO2 is blown off by hyperventilation to stop ketoacidosis.  Hypoventilation if pH is too elevated.

4) Renal Control:

If acidosis:

Excrete H+ (acid released in urine),

retain bicarb (to increase alkalinity).

Metabolic Acidosis CAUSES:

1) Seen in DM & starvation

2) seen in shock

3) ingestion of....

4) 2 reasons for H+ excretion...seen in....

**ALL of these causes result in an increase of....

Metabolic Acidosis CAUSES:

1) Seen in DM & starvation - Ketoacidosis

2) seen in shock  - Lactic acidosis

3) ingestion of ammoniom chloride

4) 2 reasons for H+ excretion: uremia, distal renal tubule acidosis  (seen in RENAL FAILURE)

**ALL of these causes result in an increase of noncarbonic acids (incr H+), elevated anion gap which is normally 10-12 mEq/L)

mnemonic for causes of metabolic acidosis with INCREASED Anion Gap (not for normal Anion Gap):

methanol ingestion,

uremia,

DKA (diabetic ketoacidosis - acute complication of DM managed with insulin),

paraldehyde,

ischemia,

lactic acidosis,

ethanol ingestion (!),

salycilic acid.

Excessive vomiting can lead to....(4 mechanisms)

Hypochloremic Metabolic Alkalosis

1) Loss of H+ = incr pH. 

2) Loss of Cl- causes incr bicarp renal reabsorption = incr pH

3) Loss of fluid leads to incr Aldosterone, Na+ renal reabsorption in exchange for H+ =

incr pH

4) Loss of K+ causes H+ influx into cells, leading to incr in plasma bicarb = incr pH.

1) resp: hypoventilation

2) renal:

-decr tubular bicarb reabsorption = bicarb excretion

- decr acid filtration = decr acid excreted in urine, more in blood.

How do anxiety attacks and/or OD-ing on antacids affect acid-base balance.

What compensatory mechanisms fixes your anxiety / antacid dosage fuck-up?

Anxious Hyperventilation / Antacid OD = alkalosis.

Renal compensation: decreased acid filtration = decr acid excreted in urine & decr bicarb regeneration.

Primary Functions of Kidney

1) removes...

2) balances...

3) releases...

4) activates...

5) controls production of....

• remove waste products/drugs from the body
• balance the body's fluids
• release hormones that regulate blood pressure
• activates vitamin D that promotes bone formation
• control the production of red blood cells

basic structural and functional unit of the kidney

Describe its 2  major components (in order, bitch) and the flow of fluid through them.

nephron

1) renal corpuscle = initial filtering component

afferent arteriole --> glomerular BP

drives water and solutes to be filtered out of the blood and into Bowman's capsule = ¨FILTRATE¨--> efferent arteriole. ...to...

2) renal tubules = reabsorption/secretion; filtered fluid converted to urine

Filtrate passes through....

1. Proximal tubule
2. Loop of Henle (thin ascending/thick descending loops)
3. Distal convoluted tubule

[image]

Glomerulur membrane (3 layers: endoth, basement, epith):

Nml function = membrane pore selectivity lets passage of small molecules; membrane lined with negative charge to prevent protein leakage.

Basement membrane disease= large blood cells/protein pass into Bowman's filtrate= hematuria/mild proteinuria.

3 factors that affect GFR:

1) this factor is controlled by autoregulation

2) this factor decreases GFR

3) this factor increases GFR

1) arterial pressure (autoregulated by RAAS)

2) afferent arteriole contriction (decr glom pressure...decr GFR)

3) efferent arteriole contriction (incr glom pressure...incr GFR initially)

GFR:

1) nml in L/day and ml/min

2) what % of filtrate is reabsorbed in tubules/passed into urine

3) what pressure in glom cap forces filtration into Bowman's

4) what pressure opposes the filtration above in q #3

1) nml 180 L/day and 125 mL/min

99% is of filtrate is reabsorbed in tubules/1% passed into urine

3) Glomerular (blood) Hydrostatic pressure in glom cap forces filtration into Bowman's

(...this pressure is greater than...)

4) blood colloid osmotic pressure (due to proteins) + Bowman's capsular hydrostatic pressure opposes filtration

[image]

Concentrations of all solutes except _______ is the same in blood and glomerular filtrate.

blood contains a much higher concentration of it.

proteins.

Autoregulation of GFR

1) what system?

2) when GFR/net filtration is low due to decr BP, the ___________ & ____________ reabsorb ______ & _________ which flow past the ____________ of the _______________.

1) RAAS

2) when GFR/net filtration is low due to decr BP, the proximal tubules & loop of Henle reabsorb Na+ & H2O which flow past the Macula Densa of the Juxtaglomerular apparatus.

[image]

Decr fluid/volume to Macula Densa

Dec stretch of juxtaglomerular receptors

Incr symp stim

= secretion of....from....

Name 3 results of this process that raise GFR

Renin from juxtaglomerular app.

(RAAS: renin>AngI>ACE>AngII>Ald>incr Na+/H2O absorption)

1) vasocontriction

2) Ald>incr Na+/H2O absorption

3) Thirst

65% of a reabsorptive and secretory processes occur here because of its high permeability: nutritionally important substances, electrolytes all have ALMOST complete reabsorption here.

this creates a osmotic gradient for the PASSIVE diffusion of .....

proximal tubule.

this creates a osmotic gradient for the PASSIVE diffusion of WATER & UREA.

The ___________ is the concentration of a substance dissolved in the blood above which the kidneys begin to remove it into the urine. When the ___(same word)________ of a substance is exceeded, reabsorption of the substance by the proximal renal tubule is incomplete; consequently, part of the substance remains in the filtrate/urine.

What is the most common reason for this?  What substance remains in the filtrate as a result?

Renal Threshold

Diabetes - glucose

Loop Of Henle (LOH)

1) 3 segments

2) as filtrate enters LOH, what is its osmolarity to plasma in peritubular capillaries.

3)Name This mechanism :  filtrate becomes progressively more concentrated as it flows down the descending loop and progressively more dilute as it moves up the ascending limb.

1) thin seg, thin descending seg, thick ascending seg

2) isoosmotic

3) countercurrent flow

Where do thiazide directics (hydrochlorothiazide) work? 

What normally happens here?

Distal convoluted tubule.

Nml function of DCT:

 - reabsorption of Na+ and Cl- (thiazides inhibit this).

- Ca actively reabsorbed (regulated by PTH & vit D)

Site where ...

1. aldosterone exerts its action on Na+/K+ reabsorption (*name the specific cell)
2. responsible for final Na conc of urine
3. K reabsorbed
4. H+ secreted/bicarb reabsorbed.

distal tubule and collecting duct

*aldosterone exerts its action on principle cells

This is where urine becomes highly concentrated, highly dilutes, highly alkaline, or highly acidic.

This is also where ____ has its effect: opening of H2O channels on luminal side of tubular cells, increasing water permeability and its movement into vascular system.

Medullary Collecting Duct

ADH (vasopressin) has its effect here: opening of H2O channels on luminal side of tubular cells, increasing water permeability and its movement into vascular system.

These agents prevent loss of K+ that occurs with the thiazide and loop diuretics:

1) ________ inhibits aldosterone mediated reabsorption of Na+ and secretion of K+

These agents prevent loss of K+ that occurs with the thiazide and loop diuretics:

1) Spironolactone inhibits aldosterone mediated reabsorption of Na+ and secretion of K+

What piece of nephron is malfunctioning?....

1) blood cells, glucose, or albumin in urine.  Serum: Creatinine/BUN increased.

2) Abnormal electrolyte panel

3) you see diluted OR super concentrated urine (specific gravity abnormal)

1) glomerulus / decr in GFR

2) Tubule

3) Collecting duct

This condition is characterized by

Azotemia (define this as well): rise in BUN & serum creatinine, decr urine outbput.

Acute renal failure - (ARF) -  (rise in BUN, serum creatinine, decr urine outbput).

Azotemia is a condition where the patient's blood contains uncommon levels of urea, creatinine, and other compounds rich in nitrogen

What is the most common form of ARF?

Characterized by...

Pre-renal failure.

Characterized by decr in renal blood flow.

Causes:

2º ischemia from pre-renal failure

insult to tubular structures (surgery)

extratubular obstruction (mass)

acute glomerulonephritis

pyelonephritis

Intra-Renal Failure/ Instrinsic parenchymal disease

(Acute Renal Failure)

Post-Renal Failure

(Acute Renal Failure)

Acute Tubular Necrosis

caused by diseases that produce a proliferative inflammatory response (endothelial, epithelial or mesangial cells) and damage the glomerular capillary wall

Nephritic Syndrome

(a glomerular disorder)

**more a result of infection (acute) eg PSGN

caused by disorders that increase the permeability of the glomerular capillary membrane, causing massive loss of protein into the urine.

Nephrotic Syndrome

(a glomerular disorder)

**more a result of chronic HTN/DM

Sx/Signs:

oliguria (little urine produced), proteinuria and hematuria, urine may become cola-colored.

Na+ and H2O are retained leading to edema and HTN

Nephritic Syndrome

(eg PSGN - inflamm response caused by immune reaction and immune complex deposition leading to swelling of glomerular capillary membrane and increased permeability to plasma prot/blood cells)

Signs/sx:

Proteinuria >3.5g/day

lipiduria

hypoalbuminemia

hyperlipidemia

General edema (H2O/Na+ retention/prot loss)

*Why hyperlipidemia?

**What 2 compensatory mechanisms cause edema?

***What are 2º complications to loss of proteins?

Nephrotic Syndrome:

(not a specific disease, but a compillation of clinical findings from increased - usu Chronic - glomerular permeability to plasma prot)

º2 to SLE, DM, membranous glomerulonephritis

*Why hyperlipidemia? lipids needed for cellular function...body makes more in compensation for loss...LDL, TGs can damage heart.

**What 2 compensatory mechanisms cause edema? Ald increase and SNS stimulation.

***What are 2º complications to loss of proteins? Thrombotic complications (DVT, PE) b/c of loss of anticoagulation protein factors as well.

You find casts in the urine.  What is your suspician/diagnosis?

1) RBC casts: where is the disorder?

2) WBC casts: significance (2).  Name 2 disorders.

3) Tubular shaped casts: name a disorder.

4) broad, waxy casts: secondary to....? seen in what disorder?

1) RBC casts: glomerular disorder.  All RBC should stay in plasma.

2) WBC casts: significance=infection/inflammation in pyelonephritis or interstitial nephritis.  THINK TUBULAR INTERSTITIAL DISEASES.

3) Tubular shaped casts: Acute tubular necrosis (due to ischemia, nephrotoxicity, tubular obstruction).

4) broad, waxy casts: secondary to collecting duct stasis.  Seen in Chronic Renal Failure

fever, eosinophilia, hematuria, mild proteinuria, and signs/sx of acute renal failure (azotemia: incr BUN/creatinine, decr urine output).

Due to....Name 3 specific causes.

Drug related hypersenitivity reaction=nephropathy.

Eg: Methicillin, Sulfonamide, Furosemide.

chronic analgesic nephritis: a nephropathy due to chronic analgesics use (ASA, acetaminophen, NSAIDs).

It is a chronic inflammatory change characterized by loss and atrophy of tubules and interstitial fibrosis and inflammation.

What drugs have the potential to damage medullary interstitial cells and inhibit protaglandin synthesis

**(Prostaglandins contribute to tubular blood flow)**

2 Common causes of post-renal failure

*in regards to the ureters, what is must happen to put a pt into renal failure?*

Post-renal failure: obstruction of urine (ureter/bladder).

causes: prostatic hyperplasia, tumors.

**bilat ureter obstruction req for renal failure**

4 mech of proteinuria

1) due to heavy exercise, fever, or orthostatic proteinuria

2) multiple myelomas

3) renal amyloidosis, glomerulonephritis

4) proteinuria >3.5g/d

1) functional - in nml kidneys, transient increase in protein excretion due to heavy exercise, fever, or orthostatic proteinuria.

2) overflow (pre-renal) - marked overprduction of a LMW protein (multiple myelomas) and exceeds nml reabsorptive capacity of proximal tubule.

3) glomerular  - renal amyloidosis, glomerulonephritis.  Results in albumin and IgG spillage.

4) heavy proteinuria >3.5g/d: nephrotic syndrome.

What test determines the concentration of urine or urine osmolarity?

Specific Gravity: determines the concentration of urine or urine osmolarity

1) Provides an index of hydration status and functional ability of kidneys to concentrate or dilute urine

2) nml= 1.010-1.025

What test reflects GFR?

1) product of

2) filtration/reabsoption/secretion in kidney

3) when serum creatinine doubles...

Serum Creatinine:

1) product of muscle metab (dependent on muscle mass)

2) freely filtered, no reabsorption, minimal secretion...if filter is damaged, levels rise.

3) when serum creatinine doubles...generally renal function has ALREADY declined by half.

Serum BUN

1) formed where, how?

2) eliminated by...

3) influenced by...

4) ratio of serum BUN to creatinine

1) formed in liver as protein metab by-product

2) eliminated by kidney

3) influenced by protein intake/hydration

4) 10:1

Endocrine: ductless glands that produce hormones that have effects on different sites

Autocrine: cell secretes hormone that binds to receptor ON THE SAME CELL and causes changes

Paracrine: affects neighboring but different cells then itself.

Hormones:

1) name 2 protein hormones

2) name 2 peptide hormones

3) name 3 adrenal hormones.  What chem class/precursor?  What other hormones have this same class/precursor?

4) name amino acid precursor and 2 hormones

5) Fatty acid precursor and 3 hormones.  What disorder and process do they appear in?

1) protein hormones: insulin, insulin growth factor

2) peptide hormones: TRH (hypothalamus), ADH

3) Adrenal hormones: mineral corticoids, aldosterone, cortisol.  Steroid hormones made from cholesterol.  Sex hormones also in this class.

4) amino acid hormones: tyrosine precursor --> thyroxin, catecholamines

5) Fatty acid derivatives/eicosanoids from arachidonic acid precursor-->prostaglandins, leukotrienes, thromboxanes.  Appear in blood disorders/inflamm processes.

Which 2 hormones modulate gene expression?

Where are the receptors?  Are they fast/slow acting?

Steroids, Thyroid

Intracell receptors

Slow acting

Which hormones are fast acting in that they activate enzymes?

Where are the receptors?

What are the 1st/2nd messengers?

Proteins, Peptides, Epinephrine, NE, Eicosanoid

Surface cell receptors

1st messenger is hormone

2nd messenger is cAMP, IP3, cGMP

Endocrine Control:

    1) 2 ways to control production

2) rate of degredation/elimination: how do you detect hormones that degrade fast?

3) 1 way to control rate of delivery

1) production regulated by direct effect & negative feedback.

2) hormones that degrade fast can be detected by tracking derivates in the blood.

3) rate of delivery controlled by up/down regulation of receptors on target cells

the production of thyroid, 2 adrenal, and sexual hormones are regulated by the negative feedback system via hypothalamus and pituitary.  Which 3 hormones don't respond to this system?  How do they respond?

Insulin and PTH respond to Ca in the blood.

Aldosterone is stimulated by K and Na.

Endocrine Disorders.

Using the thyroid gland as an example, state the heirarchy/neg feedback chain.

1) name a primary endocrine disorder.  Where is the disease?  State the levels of the hormones involved.

2) name a secondary endocrine disorder. Where is the disease?  State the levels of the hormones involved.

3)name a tertiary endocrine disorder. Where is the disease?  State the levels of the hormones involved.

Hypothalumus (TRH) --> Pituitary (TSH) --> Thyroid (T3/T4)

1) Primary dis: graves disease (hyperthyroidism).  High T3/T4, low TRH, low TSH.

2) secondary dis: pituitary adenoma.  High TSH, high T3/T4, low TRH.

3) tertiary disease: problem w/ hypothalamus.  High TRH, high TSH, high T3/T4.

What are 4 hormones that increase blood sugar? (*THIS IS ON EXAM)

What hormone lowers sugar?

Glycemia increasers: growth hormone, cortisol, glucagen, catecholamines (epinephrine/NE)

decreaser: insulin

FYI *Hyperglycemia is a slow death BUT hypoglycemia kills you fast...this is why there are so many more glucose-raising hormones, to prevent death from hypoglycemia.

Thyroid hormones (T3/T4) are responsible for...

In graves and hashimotos, what happens?

anabolic growth.

graves hyperthyroidism, excess T3/T4 results in catabolism.

hashimotos hypothyroidism = no anabolic growth.

PTH

1) how many parathyroid glands are there?

2) relation to Ca, phosphate, and vit D

4 parathyroid glands.

PTH increases Ca and decr Phosphate.  Acts with vit D.

Adrenal Gland.

Cushings = hypercortisolism

Conn Syndrome = hyperaldosteronism

Pituitary Gland

1) location and relation to vision

2) anterior gland function

3) posterior gland function

1) sella tursica w/ optic chiasm: tumor can cause tunnel vision.

2) deposit of hypothalamus hormones.  It contains releasing/inhibiting hormones

3) posterior pit: secretes oxytocin and ADH

ADH dysfunctions

1) disease of...

2) in strokes and malignancies...

3) with CNS or nephrogenic problems...

1) disease of posterior pituitary

2) SIADH (synd of innappr ADH secretion)

3) diabetes insipidus results in high volume of dilute (hypoosmolar) urine production and lots of thirst.

This hormone, released by post pituitary, stimulates pregnant uterus contractions and galactaphore canals for milk production.  It has no effect on men.

Anterior Pituitary Disorders: state the hormones produced in response to the listed hypothalamus hormones (TRH, CRH, GnRH).  State what happens with high/low levels of the Ant Pit hormone.

1) in response to TRH (thyroid-releasing hormone)

2) in response to CRH (Corticotropin-releasing hormone)

3) in response to GnRH (gonadotropin-releasing hormone)

TRH regulates TSH: secondary hypo/hyperthyroid disorders

CRH regulates ACTH (Adrenocorticotropic hormone): low levels=life threating; excess= ectopic (neoplasms)

GnRH regulates FSH/LH (which are gonadotropins):

normally, FSH stimulates ovulation/spermatogenesis & LH stimulates estrogen/testosterone production.

Deficiency=delayed puberty, infertility, hypogonadism (*OCPs inhibit LH).

Excess levels post menopause because body is trying to stimulate ovaries that are already dead.

What hormone stimulates ovulation/spermatogenisis?

What hormone stimulates estrogen/testosterone production?

List the chain of stimulation/secretion from hypothalamus to target organ.

FSH (follicle stim hrmn) stimulates ovulation/spermatogenisis

LH (lutenizing hrmn) stimulates estrogen/testosterone production

*both are gonadotropins*

Secreted from ant pituitary in response to GnRH:

Hypothalamus (GnRH) -->

Ant Pit (FSH/LH) -->

gonads (reproductive system growth/sex hormone production)

_____________ of anterior pituitary is rare.

____________ can affect an individual hormone or several hormones.  Causes: pituitary adenoma, Sheehan syndrome, stroke.  State the order of hormone losses and which 2 have the most dangerous medical consequences.

HYPERFUNCTION of anterior pituitary is rare.

HYPOFUNCTION can affect an individual hormone or several hormones.  Causes: pituitary adenoma, Sheehan syndrome (post pardum), stroke. 

Order of hormone losses: GH, FSH/LH, *TSH, *ACTH

**most dangerous medical consequences=lack of TSH & ACTH.

This hormone affects mammary gland dev, milk production, reproduction.

What inhibits its secretion (negative regulation)?

What stimulates its secretion (positive regulation)?

Excess production is the most common effefct of a ___________.  In women, this causes..(2)..In men, this causes..(3)...

Prolactin affects mammary gland dev, milk production, reproduction.

negative regulation: dopamine from hypothalamus

positive regulation: TRH from hypothalamus

Excess production is the most common effect of a pituitary adenoma.

• In women, this causes amenorrhea,     galactorrhea.
• In men, this causes hypogonadism, ED, gynecomastia.

What are the most common non-hormonal causes of ED?

If pt is over 40years, what should you consider?

ED: depression, HTN, CAD, DM

over 40: consider excess prolactin from ant pituitary adenoma causing hypogonadism, ED, gynecomastia.  ***ASK ABOUT VISION CHANGES (pituitary located in sella tursica with optic chiasm and tumors can produce tunnel vision).

Growth Hormone

1) secreted by...

2) direct effect on...resulting in...

3) indirect effect on....

4) positive regulators

5) negative regulator

6) deficiency of GH

7) excess GH

Growth Hormone

1) secreted by ant pit

2) direct effect on liver resulting in IGF production.

3) indirect effect on bone, muscle, adipose

4) positive regulators: stress, exercise, sleep, fasting, GHRH

5) negative regulator: somatostatin

6) deficiency of GH: stunted growth, dwarfism.

7) excess GH: gigantism, acromegaly.

What is the difference between human growth hormone (HGH) deficiency dwarfism and Thyroid hormone deficiency dwarfism?

HGH dwarfs have nml IQs.

Thyroid dwafs have mental retardation.

Ca

1) what % in bone

2) active form

3) inactive form

4) regulation

5) absorption, stores, elim

Ca

1) what % in bone: 99%

2) active form: free Ca ion (50%)

3) inactive form: bound to prot in plasma

4) regulation: PTH (directly related)

5) absorption (small intestines), stores (bone), elim (stool/urine)

Phosphate (anion)

1) Where is the majority located? %?

2) control of elim and abs

1) 85% in bone

2) Elim (via urine): PTH stimulates renal elimination

Calcitrol (activated vit D) stimulates absoption

Magnesium

Hypermagnesemia is rare.

Hypomagnesemia assoc with hypocalcemia (must fix mg level before Ca tx works)

PTH

1) stimulated by

2) for proper activity, needs the presence of...

3) activates

4) increases

1) stimulated by low Ca

2) for proper activity, needs the presence of vit D & Mg

3) activates calcitrol in kidney which increases GI absorption of Ca

4) increases tubular reabsorption of Ca

What raises both Ca and phosphate serum levels?

what is its main role?

Calcitrol (vit D3) - activated vit D

Main role: balance Ca/Phos to support bone mineralization.

Secreted in response to hypercalcemia.  Its role is to decrease Ca serum by supression of renal Ca abs and inhibition of bone resorption.

Used as a tx for....

Calcitonin (CT)

tx for osteoporosis.

GI

Bone

Kidney

acid-base disoder

plasma prot conc

plasms phosphate level (inversly related to Ca and PTH)

• #1 primary hyperparathyroidism
• #2 malignancy (tumors that secrete PTH-like substance)
• multiple myeloma (plasma cell disorder)
• granulomatous dis: sarcoidosis/TB
• metabolic acidosis (increased ionized calcium from reduced protein binding)

Sx:

• weakness
• N/V,
• constipation,
• anorexia,
• mental status alteration (from neurotransmitter interference)
• ECG: short QT

• hypoparathyroidism (or PTH resistance)
• vit d def (malabs, renal failure, liver dis)
• hypoalbuminemia
• alkalosis (reduced ionized calcium from increased protein binding)

Sx:

-Positive Chvostek sign* what is this?

-Positive Trousseau sign* what is this?

-laryngospasm

-HF

-Depression/confusion

-ECG: long QT

Hypocalcemia:

*

The Chvostek sign - the facial nerve is tapped at the angle of the jaw (i.e. masseter muscle), the facial muscles on the same side of the face will contract momentarily

Trousseau sign of latent tetany This sign may become positive before other gross manifestations of hypocalcemia such as hyperreflexia and tetany, but is generally believed to be more sensitive than the Chvostek sign for hypocalcemia.  To elicit the sign, a blood pressure cuff is placed around the arm and inflated to a pressure greater than the systolic blood pressure and held in place for 3 minutes. This will occlude the brachial artery. In the absence of blood flow, the patient's hypocalcemia and subsequent neuromuscular irritability will induce spasm of the muscles of the hand and forearm. The wrist and metacarpophalangeal joints flex, the DIP and PIP joints extend, and the fingers adduct.

Increased PTH, increased serum Ca.

Cause (2)

Effect (3)

Primary hyperthyroidism (adenoma, mult endocrine neoplasia)

Effect: hypercalcemia, kidney stones, decalcification of bones

decr serum Ca, increased PTH

Cause (2)

Secondary Hyperparathyroidism: diet def in Ca or vit D...or exc Phosphate.

More common cause= renal failure.

Vit D def: impaired mineralization = soft bones.

Causes: receptor resistance, low sun exposure (sunblock or pollution), severe liver/kidney dis