Patho DEck

Question 1

Describe the Renin -angiotensin II pathway

Answer 1

1. Whenever there is a decrease in blood pressure/blood volume, or a decrease in sodium ion concentration renin is secreted from the kidneys.
2. Angiotensinogen is produced in the liver and renin converts angiotensinogen into angiotensin I
3. Angiotensin I gets converted to angiotensin II in the lungs where there is high amounts of ACE (angiotensin conveting enzymes)
4. Angiotensin II is the active form of angiotensin and works in a couple of different ways to increase blood pressure
5. First it causes direct vasoconstriction of arterioles to increase blood pressure
6. It also goes to the adrenal cortical cells, specifically the zona glomerulosa, where it causes the release of aldosterone.
7. Aldosterone works by reabsorbing sodium ions in the kidneys, it also works to reaborb water via osmosis. Aldosterone also works to eliminate both potassium and hydrogen ions into the urine.
8. The increase in sodium ions and increase in blood pressure from angiotensin II and renin cause a normal blood pressure to resume which further inhibits the secretion of renin.

Question 2

Describe the regulation of calcium ions in the blood from PTH and Vitamin D

Answer 2

It is important to understand both Vitamin D and PTHs role when talking about the regulation of calcium ions

First Vitamin D conversion into the active form.

1. Dietary intake of vitamin D3 or exposure of the skin to UV light allows for cholecalicferol (inactive form of D3) to be released into the blood.
2. Cholecalciferol is coverted to calicidiol by the liver and then is released into the blood
3. Calicdiol travels to the kidney where it is converted into calcitriol (the active form of vitamin D3)

Calcium regulation

1. Whenever there is low calcium in the blood, the parathyroid receptors sense a low serum Ca2+
2. In response to a low calcium in the blood PTH is released into the blood.
3. PTH goes to the kidneys and amplifies the conversion of calicidiol to calcitriol producing much more of the active form of vitamin D3.
4. Calcitriol will then act on the GI tract to increase calcium absorption from digested food.
5. calcitriol and PTH will work on the kidneys to reasborb Ca2+ back into the blood decreasing Ca2+ loss in the urine.
6. Calcitriol and PTH will also work on the bones to increase osteoclast activity. Osteoclast activity causes bone resorbtion resulting in Ca2+ release from the bone and into the blood stream
7. Together these three effects all work to increase calcium concentration in the blood. A higher calcium concentration in the blood works in a negative feedback loop on the parathyroid gland to stop the production of PTH.

Question 3

Describe the growth hormone loop.

Answer 3

1. The hypothalamus is the starter of the growth homrone loop becuase it detects changes in time of day, age, nutrient levels in the blood, and stress and exercise
2. In response to these various stimulies, the hypothalamus releases GHRH growth hormone releasing hormone.
3. Growth hormone releasing hormone travels to the anterior pituitary via the hypothalamo-hypophyseal portal system. This causes the release of GH
4. GH released from the anterior pituitary travels to the liver where it stimulates hepatocytes to release insulin-like-growth factor, IGF-1.
5. Both IGF-1 and growth homrone stimualte target cells
6. Target cells include
   
   1. Adipose connective tissue
      
      1. They cause lipolysis
      2. They inhibit lipogenesis
   2. Liver tissue
      
      1. Stimulating gluconeogenesis and glycogenolysis
      2. inhibiting glycogenesis
   3. Bone, muscle, and all cells
      
      1. Stimulate increased growth by increased amino acid uptake which results in protein synthesis
      2. Also stimulate cellular division and cellular differentiation.
7. Net effect of Growth hormone and IGF-1 on target cells is to increase protein synthesis, cellular division, and cell differentitation. Especially in the cartilage, bone, muscle, and also causes the release of stored nutrients into the blood.
8. High levels of GH and IGF-1 cause negative feedback on the anterior pituitary inhibiting more release of GH, and negative feedback on the hypothalamus preventing the release of more GHRH.

Question 4

Describe the Thyroid Hormone feedback loop

Answer 4

1. The hypothalamus is stimulated by one or more of the following
   
   1. decreased thyroid hormone
   2. other stimuli including cold weather, pregnancy, high altititude, and hypoglycemia
2. In response to these stimuli the hypothalamus releases TRH (thyroid releasing hormone).
3. TRH travels in the hypothalamo-hypophyseal portal system to the anterior pituitary where it stimulates the anterior pituitary to release TSH.
4. TSH is then released from the anterior pituitary and travels to the thyroid gland.
5. TSH causes the thyroid galnd to release thyroid hormone into the blood. Thyroid hormone then has the following effects on the target cells
   
   1. Heart
      
      1. increase heart rate, increase force of contraction
   2. Lungs
      
      1. Increased breathing rate
   3. Together the heart and the lungs increase in respone to help meet increased oxygen demand for aerobic cellular respiration
   4. Adipose connective tissue
      
      1. increased lipolysis
      2. decrease lipogenesis
   5. Liver tissue
      
      1. increase gluconeogenesis, increase glycogenolysis
      2. decrease glycogenesis
   6. all cells, especially neurons
      
      1. increased metabolic rate
      2. increased glucose uptake
6. The net effect of thyroid hormone on the effectors is to increase metabolic rate. This is supported by the increased release of nutrient molecules and increased delivery of O2 from the heart and lungs.
7. TH levels increase, inhibiting the release of TRH and TSH.

Question 5

Describe the loop of cortisol

Answer 5

1. The hypothalamus detects stimulus or changes such as negative feedback by cortisol, time of day, and stress.
2. In response to the various stimuli the hypothalamus releases CRH (corticotropin releasing hormone) into the hypothalamo-hypophyseal portal system.
3. CRH travels to the anterior pituitary where it causes the release of ACTH.
4. ACTH travels to the adrenal glands and stimulates the release of glucocorticoids from the zona fasciculata. Specifically cortisol.
5. Cortisol has the following effect on target cells
   
   1. Liver
      
      1. increased glycogenolysis and gluconeogenesis
      2. decrease glycogenesis
   2. adipose tissue
      
      1. increased lipolysis
      2. decreased lipogenesis
   3. all cells
      
      1. stimulation of protein catabolism (occurs in all cells except hepatocytes)
      2. decrease glucose uptake
   4. Effectively, high doses of cortisol increase retention of sodium, water, decrease inflammation, suppress the immune system, and inhibit connective tissue repair
   5. The net effect of cortisol is in an increase in all nutrients in the blood.
   6. High cortisol levels inhibit the release of CRH from the hypothalamus and inhibit the release of ACTH from the anterior pituitary.

Question 6

Describe the loop of insulin

Answer 6

1. The pancreas senses an increase of blood glucose levels in the blood.
2. Beta cells within the pancreas detect the increase in blood glucose. This causes the release of insulin from beta cells.
3. Insulin stimulates target cells
   
   1. Most cells
      
      1. increases uptake of glucose by increasing glucose transport proteins in the plasma membrane
   2. all cells (especially muscle)
      
      1. increased uptake of amino acids, which stimulates protein anabolism
   3. Adipose connective tissue
      
      1. increased lipogenesis
      2. decrease lipolysis
   4. liver
      
      1. increased glycogensis
      2. decreased gluconeogenesis and decreased glycogenolysis.
4. The net effect is decrased blood glucose levels, decreased fatty acids levels, decreased amino acid levels
5. Insulin secretion is then decreased as blood glucose levels go back to normal.

Question 7

Describe the loop of glucagon

Answer 7

1. A decrease in blood glucose is detected by the pancreas
2. the alpha cells in the pancreas detect a decrease in blood glucose. This causes the release of glucagon from the alpha cells
3. Glucagon stimulates target cells
   
   1. Liver
      
      1. increased glycogenolysis
      2. increased gluconeogenesis
      3. decrease glycogenesis
   2. adipose connective tissue
      
      1. increase lipolysis
      2. decreased lipogenesis
4. the net effect is increased blood glucose and fatty acid levels.
5. As blood glucose levels return to normal the release of glucagon is increased to normal.

Question 8

What do defects in the neural tube development produce?

Answer 8

Produce anecephaly and spina bifida

Question 9

What is spina bifida?

Answer 9

• A neural tube defcet
• On a specturm - occulata common
• Most severe casese
  
  • inability to walk
  • bladder and bowel control issues
  • hydrocephalus
  • tethered cord
  • latex allergy
• Causes:
  
  • familal
  • folate insufficiency while pregnant
• Amniocentesis - shows elevated alpha fetoprotein - can be diagnostic
• Not related to pilonidal sinus

Question 10

What is arnold chiari malformation?

Answer 10

• Downward displacement of the cerebellar tonsils through the formane magnum.
• Get a non-communicating hydrocephalus
• Often have headaches aggravated by valsalva maneuvers
  
  • tinnitus
  • lhermitte’s sign - sign of pressure on the spinal cord
  • vertigo
  • muscle weakness
  • restless leg syndrome
  • paralysis
  • syrinx may form - hollow tube, can enlarge and crowd fibers in the spinal cord.
    *

Question 11

What is syringomyelia?

Answer 11

• Syringe spinal cord
• A chronic progressive degenrative disorder.
• CSF cyst in the central canal of the cord enlarges
  
  • get pain,
  • muscle weakness
  • numbness
  • stiffness
• Encroaches in the central cord
  
  • lose pain and termperature sensation in the upper extremity.

Question 12

What are signs of increased intracranial pressure?

Answer 12

• papilledema
• headache, projectile vomiting without nausea
• sinus bradycardia, hypertension
• potential for herniation

Question 13

what are causes for cerebral edema? Intracellular vs extracellular

Answer 13

• Intracellular: water moves into cells- dysfunctional Na/K ATPase pump
  
  • get a global hypoxia
  • hyponatrenmia causing osmotic shift - inappropriate ADH secretion
• Extracellular: increased vessel permeability (vasogenic)
  
  • acute inflammation -meningitis, encephalitis
  • tumor, trauma, lead poisoning

Question 14

What are signs of cerebral herniation?

Answer 14

Multiple locations of different herniations and different symptoms associated with each.

• Cingulate gyrus herniation –> compresses anterior cerebral artery and caueses an infarct and edema
• Uncal herniation – also called transtentorial herniation
  
  • get compression of CN III, fixed and dilated pupill, eye deviated down and out

Question 15

What is hyrdocephalus?

Answer 15

• Hydrocephalus is an enlargement of the ventricles in the brain. “water on the brain”
• Causes:
  
  • communication (non obstructive) hydrocepahlus
    
    • increased CSF produciton
    • decreased reabsorption via arachnoid villi
    • meningitis
    • tumor
    • SAH
  • Non communicating-Obstructive
    
    • stricture of aqueduct of sylvius - most common cause in newborns
    • tumor of the 4th ventricle
    • scarring at the base of the brain.

Question 16

What is hydrocephalus ex Vacuo?

Answer 16

When you get a hydrocephalus due to a decrease in brain mass. This is secondary to atrophy and seen in alzheimer’s disease.

Question 17

what is normal pressure hydrocephalus? how does it present?

Answer 17

This is symptomatic hydrocephalus

caused by a decrease in absorption of CSF. This is either idiopathic, secondary to a SAH, trauma, meningitis, prior intracranial surgery

There is a high pressure in the CSF. Patient presents as wacky, wobbly, and wet. Dementia, ataxic gait, urinary incontinence.

Treatable form of dementia. Treated with ventriculoperitoneal shunt.

Question 18

Abscesses, axial vs extra axial?

Answer 18

1. Abscesses are mostly caused by bacterial infections.
2. Axial
   
   1. in brain or s.c
      
      1. abscess usually has thin wall called the phlegmon. the inside grows puss. Have to use surgery to drain them.
3. extraxial
   
   1. external to brain or s.c
4. types
   
   1. epidural
      
      1. may bridge dura into subarachnoid space and brain
   2. mastoiditis –> epidural –> thrombosis of sigmoid sinus –> intracranial abscess

Question 19

How does AIDs manifest in the CNS?

Answer 19

• Aids mainests by direct cytotoxic effects on the CNS cells causing HIV encephalopathy, aspeptic meningitis, encephalitis, myelopathy, peripheral neuropathy, AIDs dementia
• Suppression of the immune system allows opportuniistic infections with other agents such as toxoplasmosis (MC), CMV, herpes simplex, JC virus (progressive multifocal encephalopathy, shingles, TB, cryptococcosis
• also causes malignancies - lymphomas 1000-4000x more common than immunocompetent population

Question 20

Eastern Equine Encephalitis

Answer 20

• Caused by the arbovirus “atrophied brain”
• Coincides with horse outbreaks
• no known cure
• supporitve measures and corticosteroids
• Presents with
  
  • high fever
  • muscle pain
  • altered mental state
  • h/a
  • meningieal irritation
  • photophobia
  • seizures
    *

Question 21

Herpes simplex encephalitis

Answer 21

• HSV-1 oral lesions - predilection for the temproral lobe. Patients present very weirdly

Question 22

Herpes Zoster/Shingles

Answer 22

• Caused by the reactivation of the chickenpox virus (varicella zoster)
• painful rash with blisters
• follows dermatomes
• Usually limited, but may become postherapetic neuralgia - months to years

tx

• Shingles vaccine is effective in about 50% of people and decreases severity is people do get it.
• Acyclovir the antiviral medicine of choice

On face - can cause ocular inflammation and blindness.

Question 23

Toxoplasmosis

Answer 23

• Toxoplasma gondi
  
  • asymptomatic or mild flu like illness
• Appears in people with weak immune system or immunocompromised
  
  • can be severe and lead to encephalitis, h/a, confusion, seizures, pulmonary infection
• Pregnancy
  
  • congential toxoplasmosos secondary to transplacental infection. Fetal death and abortion. Chorioentitis, Neurological deficits
  • precautions: screening, hygiene (cats)

Question 24

Define meningitis, encephalits, myelitis, myelopathy.

Answer 24

• Meningitis: acute infection and or inflammatoin of the meninges, especially the pia and arachnoid
• encephalitis: acute infection and or inflammation of the brain
• myelitis: acute infection and or inflammation of the spinal cord
• myelopathy: any neurological deficit in the spinal cord
  *

Question 25

Meningitis

Answer 25

• Types
  
  • bacterial
  • viral: fecal oral spread
  • fungal
  • parasitic
  • non infectious
• Note: aseptic meningitis or sterile meningitis is a meningitis in which there is a source of infection, but it is not a pyogenic (pus forming bacteria)
  
  • Examples are TB and viruses
• Spread:
  
  • hematogenous is most common
  • traumatic implantation
  • local extension from sinusitis and mastoiditis
• s/s
  
  • fever, nuchal rigidity, h/a
• dx
  
  • spinal tab
    
    • shows increased CSF protein
    • normal to slightly increased
      
      • neutrophils predominate in the first 24-48 hours then lymphoctyes after 48 hours
    • increased CSF protein
    • negative gram stain

Question 26

What meningitis present in newborns?

Answer 26

• group b streptococci
• E. Coli
• listeria monocytogenes - transmitted from mother

Question 27

What types of meningitis present in older children

Answer 27

neisseria meningiditis - menigococal

strep pneumo

hemophilus influenza type B -HIB

Question 28

What is waterhouse-friderichesen syndrome aka hemorrhagic adrenalitis

Answer 28

• a complication of meningococcal meningitis.
• Infection travels to blood stream and causes the adrenal gland to shutdown secondary to hemmorhage
  
  • caused by neisseria meningitidis, but other bacteria such as p. aeruginosa, s pneumo, tb, h flu, cmv can all cause it.

Question 29

What are causes of viral encephalitis?

Answer 29

Abroviruses: west nile virus - mosquito vector, bird reservoir

cytomegalovirus- may be neonatal, new borns, developmental disabilities, death

herpes simplex virus - temporal obes - hemorrhagic necrosis

HIV - aids dementia

Lymphocytic choriomeningitis ( endemic in mouse population)

poliomyelitis: encephalitis and myelitis (S.C) primarily a lower motor nueron disease

Question 30

What can rabies cause?

Answer 30

Can cause viral encephalitis

found in racoons (40%), dog, skunk, bat, coyote. can get from bite, and virus moves up axon to the CNS

Long incubation - 10-90 days

fever, and parasthesias at wound side

Hydrophobia: secondary to spasms of throat muscles when swallowing

flaccid paralysis and then death. Universally fatal if not treated

passive (immune globulin in wound site and active immunizatoin (human diploid vaccine)

Question 31

What is subacute sclerosis panencephalitis?

Answer 31

A rare viral encephalitis that is a slow virus, secondary to chronic persistant infection with measles (rubeola) virus

Can be managed with immunomodulator interferon and specific antiviral ribavirin, and requires lifetime treatment.

Death in 1-2 years without treatment

Question 32

What is encephalopathy?

Answer 32

A disorder of the brain, syndrome of the brain dysfunction

Get an altered mental state, loss of cognitive function, personality change, lethargy, depressed consciousness, involuntary movementes, asterixis, nystagmus, tremor, seizures

Tons of causes

Question 33

What is hepatic encephalopathy?

Answer 33

• Encephalopathy secondary to liver failure
• In advanced stages called hepatic coma or coma hepaticum
• People become forgetful, confusion, irritability, asterixis, inverted sleep pattern, lethargy, personality changes, somnolenge, clonus, progression to coma, cerebral edema, and then death
• Remember patient is in liver failure and will have jaundice, ascities, peripheral edema, GI bleeding.
• Cause
  
  • An accumulatino of toxic substances in the blood stream that are normally removed by the liver
  • 1) excessive nitrogen load: especially proteins in the intestine (from bacteria, food, GI bleeding etc) are normally metabolized in the liver
    
    • Metabolism of proteins produces amino acids and ammonia which is toxic. The ammonia is then detoxified normally into the less toxic urea and uric acid via the urea cycle and these are excreted immediately via kidneys.
    • In liver disease, ammonia is accumulated, and crosses the BBB, swelling astrocytes and causing edema. Accumulation will be aggravated by renal failure
  • 2) Electrolyte or metabolic distrubances
    
    • hyponatremia, hypokalemia secondary to diuretics
  • 3) medications/drugs: sedatives, narcotics, antipsychotics, alcohol can aggravate
  • 4) infections: pneumonia, urinary tract infection, and bacterial peritonitis

Question 34

Multiple sclerosis characteristics

Answer 34

1) Plaques - primarily in the white matter, essentially scars, ie. multiple sclerosis
2) inflammation
3) destruction of myelin sheaths - demyelination caused by a loss of oligodendrocytes - cell responsible for creating myelin sheath. loss of myelin sheath and breakdown of neural axons menas that electrical signals are no longer conducted.

• MS is an inflammatory demyelinating disease •
• MS is characterized by symptoms separated by time and location (space) •
• MS is characterized by ovoid shaped white matter periventricular T2 hyperintensities •
• Some lesions may enhance showing active inflammation •
• The course of the disease may be remitting, relapsing, progressive, or a combination

Question 35

Creutzfeld-Jakob Disease

Answer 35

A degenerative neurological disease that is invariably fatal

Not the same as mad cow disease

Caused by prion, PrP prion protein.

As a result of the prion “infection” spongiform chagnes occur as well as amyloid acumulation

• Prions are “normal” specific proteins that are abnormally misfolded and can self replicate by inducing abnormal folding of similar specific normal cellular proteins. These pathologic agents produce progressive neurodegenerative disorders by. –
• These prions induce formation of a protein polymer called amyloid which then accumulates causing degenerative brain disease by disrupting neuronal function. –
• Cannot be killed by standard sterilization techniques.

Question 36

What is the fast exam?

Answer 36

FAST•

F = Face drooping. Have patient smile. Does one side of the FACE droop?

•A = Arm weakness. Have patient raise both ARMS. Does one arm drift downward? •

S = Speech difficulty. Have patient repeat a simple phrase (“You can’t teach an old dog new tricks”). Is their SPEECHslurred or strange? •

T = Time to call 911. TIME is of the essence. If you observe any of the above signs, call 911 immediately.

Question 37

How do you distinguish between a hemorrhagic and ischemic stroke?

Answer 37

Do a CT without contrast

Question 38

What is the Penumbra?

Answer 38

It is the area of ischemia in an ischemic stroke, with still viable cerebral tissue, at the edge of a non-viable infarcted area

This is salvageable by opening up the obstructed artery with thrombolytic therapy

This is the rationale for evaluating strokes quickly

Question 39

What is the triple CT?

Answer 39

1) Non contrast CT. CT is the gold standrad for the prescence of hemorrhage. is there hemorrhage? where is the ischemia?
2) Perfusion study- creates a map of brain perfusion. Inject idodinated contrast agent and evaluate blood flow to areas of the brain. Get a MTT, CBV, CBF
3) Vascular anatomy - CT angiography

Question 40

What does a vertebrobasilar stroke cause?

Answer 40

• 9th, 10th, and 11th bulbar paralysis. Also can affect the pyramids

Question 41

Chronic traumatic encephalopathy

Answer 41

• Neurodegenerative disorder caused by “cumulative- long term neurological consequences of repetitive brain concussive and sub-concussive blows to the head”
• Characterized by delayed (8-10 years later) cognitive decline, deteriorating executive function, mood and behavioral disorders, impulsive behavior, depression, apathy, dementia (dementia pugilisitica) and Parkinsonism •
• Pathologic evaluation shows a tauopathy, neurofibrillary tangles and glial tau inclusions preferentially in cortical sulci, medial temporal lobe, structures lateral to the third ventricle, and brainstem
• NOTE: accumulation of abnormal TAU PROTEIN TANGLES

Question 42

Decerebrate vs decorticate

Answer 42

1. Extensor respsone to painful stimuli- decrerebrate posturing/response - adduction of the arms, internal rotation of the shoulder, pronation of the forearm, elbow extension, flexion of the forearm, and wrist, plantar flexion of the foot.
2. Abnormal flexor response - decorticate posturing response - flexion of forearm and wrist, clenched fists

Question 43

What does the anterior pituitary secrete?

Answer 43

ACTH

TSH

FSH

LH

GH

Prolactin

Question 44

What does the posterior pituitary secrete?

Answer 44

oxytocin

vasopressin - antidiuretic hormone >> diabetes insipidius

Question 45

What are the three categories of pituitary tumors

Answer 45

Tumors are subdivided into secretory (functioning), nonsecretory, other sellar and parasellar tumors

• Adenomas can be microadenomas and macroadenomas. small non-secretory of no clinical significance are common and considered benign.

Question 46

What is the w/u for a pituitary adenoma

Answer 46

• H&P, laboratory evaluation to exclude hypersecretion and hyposecretion of pituitary hormones, ie prolactin, IGF-1, ACTH, early morning cortisol, TSH, Free T4, LH, FSH, and testosterone.

Question 47

What is the most common pituitary adenoma? What is the most common cause of hypopituitarism?

Answer 47

• Benign adenomas are MC 65%
• invasive adenoma 35%
• Carcinoma 0.1-0.2%
• May occur in as many as 15% of population
• Macroadenomas are the MCC of hypopituitarism.

Question 48

What is a craniopharyngioma

Answer 48

A bening squmous and columnar epithelial tumor arising from the rathke cleft (embryonic precursor of the adenohypophysis)

Can act like malignant tumors with recurrances and metastases

Enlarged sellar or suprasellar masses usually solid and cystic in nature

Question 49

What happens in exopthalmos?

Answer 49

This is an autoimmune reaction direted at orbital fibroblasts

Determinants common among orbital and thyroid antigens may initiate hypersensitivity reactions that result in orbital changes

Increased hyaluronic acid increases osmotic load and passive swelling of tissues.

Question 50

How do you know if thyroid nodules are benign or malignant? what are the most common thyroid cancers?

Answer 50

• Common by ultrasound evaluation
• Clinically palpable in about 4-7% of patients
• only 5-10% of thyroid cancers are clinically palpable

Benign or Malignant?

Ultrasound can tell if lesion has cystic or solid components. •

Are all cystic lesions benign? No, but vast majority are benign •

Are all solid lesions malignant? Majority are benign. •

Can ultrasound exclude malignancy? No •

How do you exclude a malignancy?? Biopsy and surgery

Differential diagnosis of a thyroid nodule

• hot (functioning) or cold (non-functioning) - ie uptake of radioisotope
• Hot nodules - typically adenomas but 4% contain tumor
• cold nodules - 16% contain tumor
• Radionuclide studies cannot differentiate between benign and malignant
• Ultrasound used to determine cystic lesion from solid lesion
  
  • Cystic lesions tend to be bening

Most common thyroid cancers?

• Follicular and papillary. Carcinomas are well-differentiated and slow growing and associated with favorable prognossis but can metastasize, found in younger patients, female>male
• Anaplastic carcinomas are aggressive and usually found in older patients 50+
• Papillary thyroid cancer - most common 75-85%
  
  • excellent prognosis
  • younger women
• follicular thyroid cancer
  
  • women over 50
  • 15% of thyroid cancers
  • 10 year survivial is 85%
• anaplastic thyroid cancers
  
  • older patients
  • very poor prognosis.

Question 51

Vast majority of thyroid (anaplastic) cold or hot?

Answer 51

cold

Question 52

Zollinger-Ellison Syndrome - Gastrinoma

Answer 52

Triad of fulmnitaing peptic ulcer disease, gastric acid hypersecretion, and non-beta islet cell tumors of the pancreas.

NM octreotide scan - binds to somatostatin receptors on cell surfaces

Question 53

What is Conn Syndrome?

Answer 53

Hyperaldosteroism

Patients with difficult to control hypertension, sometimes early onset hypertension such as a 30 year old with hypertension

Tumor secretes aldosterone. Aldosterone works to reabsorb Na+ into the blood and excrete potassium and hydrogen. Get an increase in blood pressure and also become hypokalemic.

Question 54

What are the three types of stimulus causing hormone release?

Answer 54

Humoral, Neural, Hormonal

Humoral - molecule (not hormone) that chagnes in the blood stream. Ex decrease in Ca2+ stimulates PTH secretion.

Neural - Neurons causing production of a hormone. Sympathetics to adrenal medulla to secrete catecholamines

Hormonal - hormone that causes and stimulates the creation/release of antoher hormone such as TSH -> TH

Question 55

What are endocrine reflexes?

Answer 55

Hormonal stimulation –> “tropic”, Regulation –> negative feedback

Neural stimulation –> action potential

Humoral stimulation –> particle concentration in the blood

Question 56

What are steroid hromones, what are their attributes?

Answer 56

• Aldosterone, androgens, caltitriol, corticosterone, cortisol, estrogens, progesterone
• these are lipid soluble, formed from cholesteorl and produced by the gonads and adrenal cortex.

Question 57

What are peptide hormones? What are their attributes?

Answer 57

• Oligopeptides (3-10aa)
  
  • oxytocin, ADH (Post pit, hypothalamus)
• Polypeptides (14-199aa)
  
  • insulin, glucagon (Pancreas)
• glycoproteins
  
  • FSH, TSH (Gonads)

These are water-soluble proteins, can’t diffuse through plasma membranes

Consist of amino acid chains into their subcateorgies depending on how many amino acids they have.

Question 58

Biogenic Amines? What are their attributes?

Answer 58

• Dopamine (PIH)
• Epinephrine
• norepinephrine
• melatonin
• Thyroid hormone - biogenic amine but acts a steroid hormone to diffuse through PM

Attributes are these are water soluble with the exception of thyroid hormone

Dervied from amino acid that is modified, ie tyrosine (cyclic in nature)