Type III

collagen of blood vessels, skin, uterus and granulation tissue

[image]

What action does the Sympathetic Nervous System have on the eyes?

The parasympathetic?

• Sympathetic : Mydriasis (d for dilation, big word, big pupil)

Parasympathetic: Miosis

[image]

What Cranial nerves innnervate the tongue in the following ways:

Taste in anterior 2/3:

Taste in posterior 1/3

Motor:

Sensation in Anterior 2/3:

Sensation in Posterior 1/3:

Taste in anterior 2/3: Facial

Taste in posterior 1/3: Glossopharyngeal

Motor: Hypoglossal

Sensation in Anterior 2/3: Trigeminal (Mandibular diision-Lingual n)

Sensation in Posterior 1/3:Glossopharyngeal

[image]

Sympathetic: more viscous secretion *think of nervous lecturer needing a lot of water*

Parasympathetic: watery secretion (to aid in mastication and digestion)

Sympathetic: relaxation (think of epi pen for asthma attacks)

Parasympathetic: Contraction (anti-parasymapthetics for asthma attacks)

Parasympathetic: Point (erection)

Sympathetic: Shoot (ejaculation)

Nictonic and muscarinic receptors are both _____ receptors.

Nicotinic receptors are specifically  _____ receptors.

Muscarinic receptors are specifically______ receptors.

both are Acetylcholine receptors

Nicotinic is a ligated Na/K channel receptor, while muscarinic are G-protein coupled receptors

[image]

Diarrhea

Urination

Miosis

Bronchospasm

Bradycardia

Excitation of skeletal muscle/CNS

Lacrimation

Sweating

Salivation

DUMBBELSS

aka muscarinic agonists

cholinomimetics: mimic ACh:directly activates receptor

Beth Can Pile Meth

Bethanachol:  activates Bladder and Bowel; tx for post op, neurogenic ileus and urinary retention

Carbachol: Copy of ACh; tx for glaucoma, IOP, pupillary contraction

Pilocarpine: tx for open and closed angle glaucoma, resistant to ACHesterase

potent stimulator of sweat, tears and saliva

Methacholine: test dx for asthma; stimulates muscarinic receptors in airway when inhaled

cholinomimetic

aka indirect muscarinic agonists

prevent the breakdown of ACh at nerve terminal: increasing endogenous ACh

Neostygmine: postop and neurogenic ileus and urinary retention, Myasthenia grais, reversal of neuromuscular junction blockade post op (No CNS penetration)

Pyridostygmine: long acting myasthenia gravis ; No CNS penetration

Edrophonium: extremely shot acting used for dx of myasthenia gravis

Physostigmine: anticholinergic (atropine overdose) toxicity ; physiologically crosses blood brain barrier

Donepizil: Alzheimer's "Done forget"

COPD

Asthma

Peptic ulcers

Atropine & Pralidoxime (2-PAM)

pralidoxime regenerates active AChesterase

Organophosphates, like insecticides (parathion) inhibit AChesterase so you get parasympathetic excess (DUMBBELSS)

An autoimmune diesase that leads to fluctuating muscle weakness and fatigue cuased by circulating antibodies to ACh recptors that block ACh from binding to the receptors

Dx: ephodrium (if symptoms improve, positve)

Tx:pyridostigmine, thymectomy, steroids, plasmaphoresis

 often pts have thymic hyperplasia, atrophy or tumor (thymoma)

crisis: weakness of respiratory muscles

[image]

ptosis that worsens throughout the day is a common manifestation, diplopia

[image]

Hot as a hare: hyperpyrexia

Dry as a bone: dry mouth, urine retention

Red as a beet: flushing (can't sweat)

Blind as a bat: cyclopegia, mydriasis

Mad as a hatter: delirium

Bloated as a toad: ileus(constipation), urine retention

tachycardia

muscarinic ANTAGONIST

used to treat:

bradycardia (beta blocker overdose ex.)

dilate pupils and produce cyclopegia for eye exams

decrease airway secretions (intubation etc..)

Atropine: bradycardia, dilation of pupils and cyclopegia for eye exams

Homoatropine:dilation of pupils and cyclopegia for eye exams

Tropicamide:dilation of pupils and cyclopegia for eye exams

Benzotropine: Parkinson's disease (Park my Benz or I benz so shaky)

Scopolamine: motion sickness

Ipratropium, Tiotropium: COPD, asthma ( I pray Tio can breathe)

Oxybutinin: reduce urgency in mild cystitis and reduce bladder spasms

Glyc-opyrrolate:  parenteral: pre-op- reduce airway secretions

oral: drooling, pepetic ulcers

Alzheimers

Huntingtons

BPH

Hyperthermia (especially infants)

Glaucoma

Elderly with delerium or dementia

Ileus or GI obstruction

Antihistamines (Diphenydramine)

Parkinson's drugs (Benzotrpine, Amantidine)

TCAs (Amitryptiline)

Neuroleptics (Haloperidol)

may all enhance the effects

HOX genes

[image]

Modafinil (psychostimulant)

with scheduled daytime naps

aka petit mal seizures

treat with ethosuximide or sodium valproate

Na (sodium)

[image]

What inhibits choline transport int the presynaptic cell?

What drives choline transport into the cell?

hemicholinium inhibits

Na is required

[image]

What happens with choline immediately after its transported into the presynaptic cell?

Acetyl CoA + choline are combined by the enzyme

choline acetyltransferase and packaged into vesicles

[image]

Vesamicol : No ami (love)"Vesicol" for Acetylcholine

[image]

Calcium

[image]

cardiac muscle contraction

vesicle release

NT release

platelet functioning

activation of clotting cascade

smooth mucle contraction

skeletal contraction

bone

......on and on and on

Black Widow spider toxin

[image]

[image]

Botulinum

CLOSTRIDIUM BOTULINUM causing descending flaccid paralysis

[image]

a-bind to ACh receptor

b-bind to ACh autoreceptor on the presynaptic cell

c- diffuse away

d- degradation by AChesterase

 Vitamin B6 (pyridoxal phosphate)

Vitamin C (Ascorbate)

know these especially and where on the timeline

know both names as well

[image]

Metyrosine inhibits Tyrosine hydroxylase

[image]

Reserpine

[image]

Calcium

[image]

Ephedrines

Tyramine
Amphetamines

think "ETA of NE is increased "

[image]

Guanethidine

Bretylium

Go Back NE

[image]

 autoreceptors:

a2 & m2:binding these on presynaptic cell inhibits more release of NE

               AT-II: autoreceptor that stimulates more release of NE

 postsynpatic cell receptor

a1, B1

reuptake into presynaptic cell

metabolized and dumped in urine

[image]

Cocaine

TCAs

What enzymes can metabolize NE, and how do they do it?

What will you see in the urine?

COMT: methylates NE

MAO: oxidizes NE

will see metabolites: VMA, Metanephrine and Normetanephrine in the urine

Gq the "Cutesy" protein for

Phospholipase C

Calcium

Protein Kinase C

Histamine-1

Alpha-1

Vasopressin-1

M1 & M3

"Gq Cutesy's HAVe 1 M&M"

vasoconstriction-->increase PR-->increase BP

mydriasis

increase intestinal and bladder sphincter contraction

[image]

Gi: inhibits sympathetic outflow

vasodilation

(remember it inhibits NE release as an autoreceptor on the presynaptic cell)

Gs-->Adenyly cyclase-->cAMP-->PKA

[image]

Match the G protein with each receptor:

alpha1

alpha2

beta1

beta2

M1

M2

M3

D1

D2

H1

H2

V1

V2

alpha1-q

alpha2-i

beta1-s

beta2-s

M1-q

M2-i

M3-q

D1-s

D2-i

H1-q

H2-s

V1-q

V2-s

"QISS (kiss) and QIQ (kick) til ur SIQ (sick) of SQS (Super kinky Sex)"

H2

D1: relax renal vascular smooth muscle

D2: modulates transmitter release, esp in brain

Describe functions of these receptors

M1

M2

M3

M1:CNS enteric ganglion

M2: decrease HR and contractility of atria

M3: increase exocrine secretions, increase gut persitalsis, increase bladder contraction, bronchoconstriction, increase pupillary sphincter muscle constriction (miosis), ciliary muscle contraction accomodation

V1:increases vascular smooth muscle contraction

V2:Increases water permeabilty and reabsorption in the collecting tubules of the kidney

Vasopressin: presses vasos (contraction) and presses in AQPs

Name the hormones that come from these glands and what they do:

Pineal:

Hypothalamus

Pituitary (distinguish Anterior and Posterior):

Thyroid

Parathyroid

Adrenal

Pancreas

Ovaries

Testes

[image]

[image]

Cortisol

[image]

Parafollicular C cells of the thyroid gland

 Calcitonin stimulates osteoblasts, decreases plasma calcium levels

[image]

FSH

LH

ACTH

TSH

MSH

CRH

B-HCG

ADH

PTH

calcitonin

GHRH

glucagon

ANP

EDRF

GnRH

ADH

oxytocin

TRH

Histamine

Gastrin

Ang II

Steroid hormones, like sex hormone testosterone, have to be bound to binding proteins to pass through blood. The bound form is inactive; therefore, increasing the amount of globulins would lower the amount of free/active testosterone in a male resulting in gynecomastia and hypogonadism

normal to high levels of TOTAL testosterone

Low levels of FREE testosterone

[image]

more free/active testosterone resulting in hursutism, irregular periods..

[image]

like most blood proteins, they are made in the Liver

[image]

What inhibits prolactin? What drug is associated with prolactin inhibition?

What can promote prolactin secretion?

dopamine (from arcuate nucleus of hypohalamus) inhibits prolactin

stress

bromocriptine is a dopamine analogue

_____________________________________

neuroleptics antagonize dopamine and increase prolactin secretion

nipple stimulation can prolactinomas can increase prolactin secretion also

What is the downstream mediator of Growth Hormone?

What inhibits GH?

downstream mediator: IGF-1

inhibitor: somatostatin

What are the embryologic origins of:
Posterior pituitary

Anterior Pituitary

Posterior Pituitary: neuroectoderm

Anterior Pituitar: Surface ectoderm (Rathke's pouch)

[image]

low levels of cortisol cause the Pituitary gland to pump out a lot of ACTH which is made in conjunction with MSH(both from POMC

[image]

"The BETA Family Love alphas"

TSH

Beta-HCG

FSH

LH

Prolactinoma

remember prolactinomas usually cause hypogonadism leading to amenorrhea and infertilty in both men and  premenopausal women

no symptoms in postmenopausal women

gynecomastia in men

rarely see galactorrhea at all

bitemporal hemianopsia

[image]

[image]

A pregnant woman comes in with skin changes seen below. What is this called and what do you tell her?

[image]

What are some clincal symptoms of acromegaly?

Acromegaly caused by excess GH in adults: coarse face, large hands and feet, increased spacing in teeth due to large tongue, deep voice, impaired glucose tolerance

[image]

Pituitary excess:Acromegaly, TSH-secreting tumor, ACTH-secreting tumor

GI endocrine excess: (Carcinoid syndrome, Zollinger-Ellison Syndrome, VIPoma, Glucagonoma, Insulinoma)

Diarrheal diseases (off label) not FDA approved

Reduce splanchnic circulation (off label): portal HTN with varices, bleeding peptic ulcers

Glomerulosa: Mineralcoritcosteroids

Fasiculata: Glucocorticosteroids

Reticularis: Androgens

[image]

What is the most common adult tumor of the adrenal medulla?

Pheochromocytoma

can cause episodic tachycardia and hypertension

most are unilateral, in adults, benign, idiopathic

look for catechlamine metablites in serum and urine: VMA, Metanephrine, HVA, Normetanephrine

Tx: alphablocker (HTN) and beta blocker (Tachycardia) together and surgery

Symptoms: sympathetic overdrive: Panic attacks, Polycythemia(increase erythropoietin), Pain (headache), Pressure (BP), Pallor, Perfusion (sweating), Palpitations (tachycardia)

[image]

[image]

ACTH: stimulates Desmolase to convert cholesterol to pregnenolone

[image]

Ketoconazole : antifungal

 inhibits cholesterol(ergosterol) formation

Acetate-->

Cholesterol

 (desmolase)

   pregnenolone

(3-beta-hyroxysteroid dehydrogenase)

Progesterone

(21-alpha hydroxylase)

Deoxycorticosterone

(11beta-hydroxylase)

Corticosterone

(aldosterone synthetase)

Aldosterone

D-3-21-11-A

Acetate

Cholesterol

(desmolase)

pregnenolone

(17alpha-hydroxylase)

17alpha-OH Pregenenolone

(3beta hydroxysteroid dehydrogenase)

17alpha-OH Progesterone

(21-alpha hydroxylase)

11-Deoxycortisol

(11beta- hydroxylase)

Cortisol

D-17-3-21-11

Acetate

Cholesterol

(desmolase)

Pregnenolone

(17alpha hydroxylase)

17alpha OH-Prognenolone

DHEA

(3beta hydroxysteroid dehydrogenase)

Androstenedione

Testosterone

(5alpha reductase)

DHT

D-17-3-5

Aromatase

estrogen is an 18 carbon molecule

Inability to produce sex hormones and cortisol and an excess of mineralcorticoid preoduction:

phenotypic female

no secondary sex characteristics

HTN

(1 in the first digit: HTN)

[image]

Inabilty to produce cortisol and mineralcorticosteroids

increased production of sex hormones

-elevated ACTH (no cortisol feedback)

-HYPOtension (no aldosterone)

-masculinization

(1 in the Second digit _ _: masculinization)

Inability to produce cortisol, aldosterone and corticosterone

increased DEOXYCORTICOSTERONE-->HTN

masculinization (increased sex hormones)

(1 in the first digit : HTN

1 in the second digit: masculinization)

senses stress by optimizing the brain function in the following ways:

upregulates alpha1 receptors in arterioles:increase blood pressure

decreases bone formation for more calcium into blood:can cause osteoperosis chronically

anti-inflammaory & immune suppression (causes rebound leukocytosis): inhibits production of leukotrienes and prostaglandins, inhibits leukocyte adhesion, blocks histamine release from mast cells, reduces eoisinophils, blocks IL-2 production

stimulate gluconeogenesis in liver but also increases insulin resistance peripherally to preserve for the brain and RBCs: can exacerbate diabetes

increases lipolysis and proteolysis for more buiding blocks for energy

decrease collagen synthesis: thin the skin

increases apoptosis

Bisphosphonates

[image]

excess cortisone.

#1 cause: steroid use

#2 cause: Cushings disease: ACTH producing tumor in pituitary

other causes: ectopic ACTH tumor (very high levels of ACTH)

(small cell lung cancer, bronchiole carcinoid tumor etc..)

adrenal adenoma secreting cortisol (low ACTH from feedback inhibition)

[image]

easy bruisability

tinninng of the skin

osteoperosis

adrenal-cortico atrophy

peptic ulcers

diabetes

immunosuppression

psychosis

insomnia

Cushing's syndome

Hydrocortisone

Prednisolone

Prednisone

Triamcinolone

Dexamethasone

Beclomethasone

long acting highlighted

Aldosterone increases sodium reabsorption and K secretion primarily at the principal cells of the collecting tubules and at the sweat glands

Increases sodium reabsorption in the gut

increases blood volume and pressure

decreases heart contractility

Sprinolactone is a K-sparing diuretic that acts as against aldosterone to prevent your body from absorbing too much salt and keeps your potassium levels from getting too low. Spironolactone is used to diagnose and treat a condition in which you have too much aldosterone in your body.

Spironolactone also treats fluid retention (edema) in people with congestive heart failure because it decreases preload

Also used in cirrhosis of the liver, or a kidney disorder called nephrotic syndrome. This medication is also used to treat or prevent hypokalemia (low potassium levels in the blood).

High K levels

Angiotensin II

Dexamethosone test

 healthy patient: cortisol is suppresed

ACTH producing pituiary tumor low dose: elevated levels remain

ACTH producing pituitary tumor High Dose:cortisol is suppressed

primary hyperaldosteronism

increased BP

hypokalemia

metabolic alkalosis

low plasma renin (negative feedback inhibition)

What is secondary hyperaldosteronism?

Treatment?

Hyperaldosteronism caused by the kidneys hyersecretion of renin bc the JGA senses low volume due to:

renal artery stenosis

chronic renal failure

congestive heart failure

nephrotic syndrome

cirrhosis

Tx: spirinolactone (K sparing diurteics/aldosterone antagonist)

A primary adrenal insufficiency disease usually autoimmune causing adrenal atrophy

sx: hypotension

hyponatremia

hyperkalemia

weakness, fatigue

Anorexia

weightloss

hyperpigentation (MHS produced in excess with ACTH)

[image]

Acute primary adrenal insufficiency due to adrenal hemorrhage associated with Neisseria Meningitidis septic shock

characterized by acute pulmonary insufficiency petechial rash and coagulopathies, DIC

Tx: Fludrocortisone and Cortisol

[image]

low cotisol

pituitary is not making ACTH

(no hyperpigmenation, no hypokalemia because you have sufficient Aldosterone-kidney can still make renin and trigger aldosterone synthesis)

Abrupt withdrawal of exogenous steroids

--hypothalamus stops making CRH, and when the person stops taking meds they wont make endogenous cortisol right away)

low endogenous cortisol levels is main clinical sign

What is the most common tumor of the adrenal medulla in kids?

What is elevated? what is the oncogene associated?

What is the tumor marker and what is seen on immunohistochemical stain?

What is sigificant histlogically?

Adrenal Neuroblastoma

can occur anywhere along the sympathetic chain

neural crest origin cell

elevated HVA

N-MYC oncogene

Bombesin tumor marker

neurofilament immunohistochemical stain

Homer-Wright Rosette (see slide)

[image]

[image]

Multiple Endocrine Neoplasias

MEN I: Pituitary, Pancreas, Parathyroid

MEN IIA: Parathyroids, Pheochromocytoma, Medullary Thyroid Cancer

MEN IIB: Medullary Thyroid Cancer, Pheochromocytoma, Mucosal Neuromas or GI tumors

[image]

[image]

MEN I: Pituitary, Pancreas, Parathyroid

MEN IIA: Parathyroids, Pheochromocytoma, Medullary Thyroid Cancer

MEN IIB:  Pheochromocytoma, Medullary Thyroid Cancer, Mucosal Neuromas or GI tumors

mostly stimulates beta receptors :

increase heart rate and contractility (beta1)

and vasodilation (beta2)

they balance each other so NO EFFECT ON BP

Stimulates alpha1 and beta1 mostly

increases heart rate & contractility

vasoconstriction

increase in BP and increase HR

given as an agent to raise blood pressure in the setting od shock, severe hypotension

primarily alpha1

vasocontriction--> elevates BP-->reflex bradycrdia

use for SEPTIC SHOCK

has beta 1 and beta 2 action

increase HR and reflexive tachycardia from vasodilation

used for AV block

not commonly used anymore

direct sympathomimetic

low dose:D1-augment renal blood flow so use in conjunction with Norepinephrine to treatment of shock to prevent renal damage (not sure if beneficial)

medium dose: D1 and Beta-1: cardiogenic shock 

high dose: D1, Beta-1, Alpha-1 vasoconstriction septic shock

primarily Beta 1- will increase contractility and HR

CHONO and IONO- tropic

cardiogenic shock

heart failure exacerbtion

cardiac stress test

alpha-1 agonist

decongestant

vasoconstriction of sinuses

can also raise BP so dont give to HTN pts.

Alpha-1 agonist

vasoconstriction of sinuses but can also

raise blood pressure so dont give to HTN pts

Albuterol

Levalbuterol

selective B2 agonists with some B1 effects

some tachycardia

Terbutaline

selective B2 agonists

they are indirect sympathomimetics and stimulate te release of stored catecholamines  (NE) into the synapse?

Excessive daytime sleepiness

obesity

ADD

Major Depressive Disorder

life DEPIND on it

Epinephrine:anaphylaxis shock, glaucoma (open), asthma, hypotension

Norepinephrine: hypotension, shock

Dopamine: shock (renal perfusion), heart failure, inotropic and chonotropic

Isoproterenol: torsade de poines, bradyarrythmias (can worsen ischemia)

Dobutamine: beta 1-heart failure, cardiac stress test, ionotropic and chonotropic

Phenylephrine: hypotension, ocular procedures, rhinitis

Salmeterol:long tem asthma, COPD

Albuterol: acute asthma

Metaproterenol: acute asthma

(SAM)

 (Slow like a Tertle Ritard)

Terbutaline: reduce premature uterine contractions

 Ritodrine:reduce premature uterine contractions

If you take these indirectly, you will ACE your exam ;)lol

Amphetamine: narcolepsy, obesity, ADD

Ephedrine: nasal decongestant, urinary incontinence, hypotension

Cocaine: causes vasoconstricion and local anesthesia *(never give with Beta blockers--can cause EXTREME HTN from unopposed alpha 1 activation)*

Clonidine & alpha-methyldopa:

alpha2 agonist: decreases central sympathetic outflow: HTN especially with renal disease bc doesn't decrease blood flow to kidneys

NE: alpha 1 agonist action causes vasoconstriction which increases both systolic and diastolic  pressures--> MAP increases-->baroreceptors fire-->reflex bradycardia

NET EFFECT: increase MAP, decrease HR

(remember NE has no B2 action)

____________________________________

Isoproterenol: Beta-1 and 2 agonist causes vasodilation -->decrease MAP-->increase HR by both beta1 and reflex response

NET EFFECT: decrease MAP, increase HR

Prazosin

Terazosin

Doxazosin

Tamsulosin* (flomax)

for HTN  and urinary retention in BPH

SIDE EFFECTS: 1st dose orthostatic Hypotension, dizziness, headache

[image]

Phenoxybenzamine(irrerversible):

pheochromocytoma

[image][image]

Phentolamine(reversible):

pts on MAOIs that eat tyramine containing foods (fermented, ripe foods)

[image][image]

side effects for both: orthostatic hypotension, reflex tachycardia

Mirtazipine: depression -specifically pts that don't sleep well or eat well bc of side effects

side effects: sedation, increased cholesterol, increased appetite

decreased blood pressure

explanation: alpha blocker will block the vasoconstiction, but Epinephrine will still bind to beta receptors. Beta 2 will cause vasodilation and decrease blood pressure while beta 1 will increase HR

none

explanation: phenylephrine mainly acts on alpha 1 receptors, so an alpha 1 blocker will simply cancel out the effects and there will be no change in BP

A BEAM

Acebutlol

Betaxolol

                              Esmolol (short acting for SVT)

Atenolol

           Metoprolol (SVT)

*these are best in pts with comorbid pulmonary disease*

applications:

angina pectoris: decreases O2 consumption

MI: decrease mortality

SVT: decreases AV conduction velocity

HTN:decrease cardiac output

decrease renin secretion

CHF: slows progression of chronic failure (wouldn't use this if acute heart failure-use the opposite like dobutamine)

What drug would you use for a pt experiencing thyroid storm?

Propanolol (nonselective Beta blocker)

"Prop the umbrella up and prepare for the storm"

[image]

Timolol

decreases secretion of aqueous humor

Propanolol

Timolol

Nadalol

Pindolol

[image]

Carvedilol

Labetalol

(vasodilatory)

strange ending bc they are strange acting

Metoprolol

Carvedilol

Myocardial Correction

Nadolol

"no quiere nadar en su sangre"

Would you give beta blockers to someone experiencing:
aortic dissection:

cocaine induced MI:

aortic dissection: Yes, decreases blood pressure

Cocain induced MI:NO, will increase the blood pressure, cocaine acts similar to Epinephrine and stimulates all adrenergic receptors, by blocking the beta receptors, you will remove beta 2 stimulation (vasodilatory) by cocaine and now be left with unencumbered alpha 1 (vasoconstriction) stimulation and an increase in BP

leptin stimulates the ventromedial nucleus

leptin inhibits the lateral area

Glossopharyngeal

CN IX

Vagus and Glossopharyngeal

CN X and IX

Facial

CN VII

it innervates these glands

Glossopharyngeal

CN IX

Glossopharyngeal

CN IX

hypoxia and blood pressure

failure of fusion of the maxillary and medionasal processes

[image]

failure of fusion of the lateral palatine processes, nasal septum, and/or the medial palantine process

hard for baby to suck-need special nipple

[image]

multifactorial

-genetic

-toxins

-folate deficiency

What would cause this:

[image]

Glossitis: think glossy tongue

Vitamin B deficiencies

Iron deficiency

Plummer-Vinson syndrome

White patch on the tongue caused by epstein barr virus

can be mistakened with thrush

[image]

aka hereditary hemorrhagic telengiectasia

AD disorder that causes lots of telangiectasias, aneuryms and Atrio-Ventricular Malformations

pts are prone to:

High output heart failure

nose bleeds

GI bleeds

Iron def

Visceral bleeds (even lung, liver, brain)

[image][image]

What drugs can cause hyperplastic gums?

[image]

HPV

(also remember tobacco and alcool increase risk)

p16

p53

Cyclin D1

dryness of the mouth

Sjorgens syndrome

autoimmune

-dry eyes and dry mouth

drugs can cause xerostomia also

dry mouth leads to cavities and susceptibilty to candida and difficulty swallowing and speaking

[image]

What organisms can cause infection if the condition in this picture is not resolved

[image]

sialolithiasis: stone in the salivary gland

staph aureus and strep viridans (mutans)

Pleomorphic adenomas

benign and likely in the parotid gland

containing mesenchymal and epithelial differentiation

[image]

2nd most common benign: Warthin cystic tumor

Coronavirus

Adenovirus

Rhinovirus

Echovirus

When you have a cold, take CARE

[image]

Nasal steroids

[image]

What is the treatment for eustachian tube dysfunction?

[image]

nasal steroids

Can you label the sinuses?

[image]

CT again of sinuses

[image]

Did you know?

[image]

What patient populations are susceptible to infection by mucormycosis?

[image]

Diabetics with DKA

Leukemia

Immunocomprimised

Trauma/burns

Malnutrition

iron overload/ deferoxamine

MEN 2A

MEN 2B

Medullary thyroid carcinoma

Papillary thyroid carcinoma

What drugs would you use for

anaphylactic shock

cardiogenic shock

septic shock

anaphylactic: epinephrine

cardiogenic: dobutamine

septic: norepinephrine

endoderm

Patient comes in with this mass in the midline that moves wih swallowing. What is the most likely diagnosis? What would you tell the pt?

[image]

Thyroglossal duct cyst

need to be rmoved because can become infected

Cretinism:

failure of bone growth: short stature

lack of CNS maturation: mental retardation

[image]

Grave's Disease

TSI stimulates the Thyroid receptor

[image]

Follicle: months

Blood: 1-2 weeks

Cells: days or weeks

growth and maturation of bone (acts synergistically with growth hormone and somatomedin (IGF-1))

maturation of CNS (perinatal)

Beta-adrenergic effects on heart

increases BMR

Increases absorption of glucose from GI

Increases lipolysis

Increases glycogenolysis

Increases gluconeogenesis

What happens to the total thyroid levels in the setting of

-hepatic failure

-pregnancy

What tes would you use to diagnose an abnormality?

hepatic failure: decreased TBG--> decreased total thyroid hormones but may have normal free hormone levels

pregnancy & oral contraceptive use: increased TBG-->increased total thyroid hormones but normal free hormone

TSH and free T4 are the two main tests to diagnose a thyroid disorder

Type III HSR

[image]

What is the classic arrhytmia with Thyrotoxicosis?

How do you treat?

Atrial Fibrillation which causes a rapid ventricular rate

Tx:

beta-blocker: Propanolol

Anti-thyroid meds:

Propylthiouracil and Methimazole: inhibit peroxidase and prevent organification

PTU: blocks peripheral conversion of T4 to T3 also

also best choice for pregnancy, less birth defects than methimazole

side effects: skin rash, aplastic anemia (one marrow suppression), agranulocytosis, hepatotoxicity

Our Method is to Prop the umbrella to Prepare for the storm. (Thyroid storm)

focal patches of hyperfunctioning follicular cells that work independent of TSH

cause of hyperthyroidism

caused by a mutation of the TSH receptor

hot nodules: on radioactive throid scan, they show an increase of radioactive iodine uptake, usuallybenign

cold nodules: malignant

[image]

THE TONGUE

[image]

Jod-Basedow phenomenon:

thyrotoxicosis in a patent with iodine deficiency goiter is made iodine replete

Thyroid tertoma

What is the most common cause of hypothyroidism?

Hashimoto's thyroidits

increased risk of non-hodgkin's lymphoma

nontender thyroid

Hurthle cells

lymphocytic infiltrate

Subacute thyroiditis (de Quervain's)

granulomatous inflammation

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Reidel's thyroiditis

cause of hypothyroidism

thyroid replaced by fibrous tissue

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In what maligancies do you see psammoma bodies?

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"Sam Makes Me Pissed"

Serous cystadenocarcinoma of ovary

Meningioma

Malignant mesothelioma

Papillary carcinoma of thyroid

Medullary carcinoma of the parafollicular C cells

see sheets of cells in amyloid

supplements sulfhydryl groups

and glutathione

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Neural tube defect

failure of fusion

Missense mutation

Electrophoresis

(+) HgA>HgS>HgbC (-)

stabalizes the lower spine and contributes to hip flexion, external rotation, side bending and raising yourself when lying on your back

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PCO2 is a potent cerebral vasodilator

cerebral vascular resistance will decrease

Succinyl CoA synthetase in the reaction that converts Succinyl CoA to Succinate

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Daptomycin is a lipopeptide antibiotic used in the treatment of systemic and life-threatening infections caused by Gram-positive organisms.

Cannot treat pneumonia because it binds to pulmonary surfactant

It inserts into the cell membrane in a phosphatidylglycerol-dependent fashion, where it then aggregates. The aggregation of daptomycin alters the curvature of the membrane, which creates holes that leak ions. This causes rapid depolarization, resulting in a loss of membrane potential leading to inhibition of protein, DNA, and RNA synthesis, which results in bacterial cell death

Golgi Tendon Organ

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Clomipramine

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Mirtazipine (Atypical antidepressant)

• α2 receptor antagonist
  • ↑ release of NE and serotonin
• 5-HT2 and 5-HT3 receptor antagonist

Spironolactone

Digitalis

Cimetidine

Chronic alcohol

Estogens

Ketoconazole

Marijuana

Tamoxifen

Clomiphene

Amiodarone

Lithium

Sulfonamides

phenytoin

verapamil

Diuretics

-Furosemide

Thiazides

Niacin

Cyclosporine

Pyrazinamide

(muscle paine and elevated serum CPK)

Fibrates

Niacin

Statins

Cochicine

IFN-alpha

Hydroxychloroquine

Glucocorticoids

Corticosteroids

Heparin

Proximal tubule defect

Expired Tetracyclines

heavy metal exposure

Wilsons disease

Bupropion

Imipinem/Cilastatin

Isoniazid

Eveninf primrose oil

Enflurane

Tramadol

Metoclopramide

ALCOHOL AND bENZO WITHDRAWL

Drink Corona at Midnight and Suffer Post Binge

Disulfuram

Cephalosporins (some not all)

Metronidazole

Sulfonylureas (1st gen)

Procarbazine

Aminoglycosides

Vancomycin

Loop Diuretics

Cisplatin

PICK EGS

Protease inhibitors

Isoniazid

Cimetidine

Ketoconazole

Erythromycin

Grapefruit juice

Sulfonamides

calcium and atropine

glucagon

Dimercaprol

Succimer

succimer, penicillamine, Dimercaprol commonly in kids

EDTA calcium for adults

Nitrites

thiosulfate

hydroxycobalamin

Fomepizole

dialysis

can also use ethanol to compete with it, but not standard

Bartholin cyst

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HPV related: dysplasia(VIN) from HPV 16 and 18 (younger women)

Non-HPV related: long standing Lichen sclerosis (postmenopausal)

PAS+ , keratin+, and S100-

sample from the vulva

extramammary paget's disease

carcinoma (no underlying cancer like yo would see in the breast)

(Melanoma would ONLY be positive for S100)

Adenosis

associated with females exposed to DES in utero

increased risk of clear cell adenocarcinoma

positive IHC staining for desmin and myoglobin

cytoplasmic cross striations

Inguinal nodes

(upper 1/3 goes to iliac nodes)