System Disease First Exam

Block action of histamine by blocking histamine receptors

High to keep effectiveness

Second generation

second generation

Becuase they not only fit into histamine receptor sites, they also fit into many other CNS receptors

MAO inhibitors act to leave more adrenergic transmitter in the synaptic cleft. Antihistamine is an anti-cholinergic. The signal amplification of the adrenergic along with the dulling of cholindergic balance will yield an adrenergic overdose

Antihistamine is an anticholinergic, which will cause pupil dilation, something you don't want with narrow angle glaucoma

No, Antihistamine causes increases of mucous secretion- somehting an asthmatic would not like

Drowsiness- caused Primarily by first generation
GI: Dry mouth and eye, nausea, diarhea, and vommitting

All first generations are dosed every 6 hours:
Diphenydramine
Chlorpheniramine

Second Generations are given once a day- something that definitely helps compliance.
Loratidine
Fexofenadine
Desloratidine
Certirizine

1. Not centrally acting so they don't produce as many side effects.
2. They also increase patient compliance with qd dosing
3. Unfortunately, they become ineffective after a month, so you have to keep switching between them

Inhibit chloride channels in mast cell cell membrane

People with asthma and allergic reaction to antihistamines

Weeks. Therefore, usually used in conjunction with anti-histamine or steroid(keeps inflammation down while mast cell stabilizers take hold)

Cromolyn sodium
Nedocromil
Lodoxamine

NSAIDS

Have the ability to reset body thermostat in the hypothalamus= fever reduction

Pain relief via prostaglandin blocking

GI problems ensue

Inhibit platelet aggregation via thromboxin A-2 blocking. Aspirin most well known. This will prolong bleeding

NSAIDS block prostaglandin synthesis, it thus shifts the eicosanoid metabolites in favor of leukotrienes which cause vasoconstriction.

Prostaglandins are integral for blood blow to the kidney. NSAIDS will decrease prostaglandin synthesis. This would be bad for a diabetic patient

CNS: HA, dizziness, insomnia, tinnitus (ASA)
GI: NV&D, anorexia, dyspepsia (digestive problems)
GU: Dysuria (pain with urination), nephritis, renal failure

Acetylsalicylic acid (Aspirin)
Ibuprofen (Motrin)
Indomethacin (Indocin)
Napoxen (Naprosyn)
Ketorolac (Toradol)
Celecoxib (Celebrex)- Selective COX-2
Valdecoxib (Bextra)

Favor- bad for diabetics

Cortisol

Turn off selective mediators (cytokines, prostaglandins, and interleukins) which will decrease circulationg lymphcytes, macrophages, and neutrophils.

Lymph tissue

Decrease the body's ability to fight infection

Erythrocytes, Platelets, and Neutrophils

Decreases (natural steroids like aldosterone and cortisol)

increase it

Suppresses functions

Increase

Slowing of a corneal ulcer would decrease scarring

wasting- something have trouble climbing steps

33%

Predisone is a prodrug which is converted to prednisolone in the liver. If a patient has decrease liver function, you would want to just give prednisolone

Cortisol

4
4
5
5
20-30

Moderate = 0.5 mg/2.2 lbs/d
High = 1 to 3 mg/2.2 lbs/d. 20-60 mg/day.
Massive = 15 to 30 mg/2.2 lbs/d

We operate in the low to high range. Anything more would must be co-managed

It is a readction to excessive amounts of Ag

Disease resulting from immune mediated tissue damaging reactions

Allergic and anaphylactic

IgE

Mast cells and basophils degranulate in response to two Fc portions of IgE binding and release histamine, arachadonic acid, platelet activating factor.

Arachadonic acid and platelet activating factor staying in the system, hurting the patient.

The hope of getting the body to produce IgG instead of IgE in response to antigen, thus disallowing Type I injuries

Ab-dependent

Ab causes complement activation resulting in lysis of cell death. This is what happens to a fetus in a mother.

Abs recruit and activate inflammatory cells (macrophages). This results in complement chemotactic factors.

Go through "frustrated phagocytosis" where they cant phagocytose, so they throw up lysosomal enzymes. An example of this is Moorens ulcer in the Cornea and conjunctival epithelean tissues

Phagocytosis of complement or Ab-coated cells (opsonins). Hemolytic anemia where the patient producs Ab to RBC

Ab- dependent cell-mediated cytotoxicity where Ab coats body tissue and Natural Killer cells destroy the tissue. Thyroiditis is an example of this

Immune comlex- mediated

Unphagocytosed Ag-Ab complexes deposit in tissue, and active complement, forming anaphlotoxins C3A and C5a.

Blood vessals and kidneys. Recall that these vessals are very similar to eachother. Also happens in the joints

1. Reactive arthritis (ReA)- Riders disease, can’t see, can’t pee, can bend a knee.
2. Systemic lupus erythematosus (SLE)- eye relation and neovascularization
3. Polyarteritis nodosa
4. Sjögren's syndrome- Destroys salivary and lacrimal glands.

Cell mediated (caused by T-Cells)

Jacob Eugene Hannon

No

1. Poison Ivy and Poison Oak
2. Type 1 diabetes mellitus
3. Multiple sclerosis
4 Inflammatory bowel disease (Crohn’s disease)
5.Rheumatoid arthritis (RA)- Could be Type III depending upon responses

2-3 days

1. Initiated by CD4+ T cells, Helper T-Cells (delayed-type hypersensitivity - DHT) Secrete cytokines to recruit macrophages
Tuberculin reaction is an example of this type of reaction. Tells whether or not someone has been exposed to tuberculosis.
2. Initiated by CD8+ T cells, Cytotoxic cells (direct cell cytotoxicity) Cytotoxic cells themselves are responsible for the damage. Found in Graft rejection

No one knows

Ab stimulate or block receptors

Grave's disease. Thyroid in constantly stimulates

Myasthenia Gravis

Type II

Hypoxia
Physical agents- heat or cold
Chemical agents and drugs
Infectious agents
Immunologic reactions
Genetic derangements
Nutritional imbalances

Yes

Up to a point yes

Shrink of cell by loss of substance. It is not death

Age, Decreased blood supply, nutrition, and stimulation.

Yes, they just require less energy to sustain

Increase structural synthesis without cells division

Hormonal (Transient): changes in breast during pregnancy
Compensatory: kidney enlargement when one is removed
Adaptive: muscle enlargement with exercise

An increase amount of cells

Hormonal: pregnancy
Compensatory: replacement of tissue

Epithelial hyperplasia, usually from things like papilloma virus

Cells switch type

Epithelial metaplasia in smoking. Destroys columnar ciliated epithlium so body switches to stratified squamous. Body can’t clear mucous as well.
Mesenchymal Metaplasia: Fibroblasts to osteoblasts.

Yes

Disorderly, non-neoplastic proliferation of cells

Architectural anarchy,
Trememendous cell and size variation

Ephithelial

An advanced form of dysplasia over the entire thickness of tissue. Pre-neoplastic

New, autonomous cell growth

1. Benign neoplasms- Usually floppy and moves around
Well-differentiated cells
Look and act like forbearers. I.E. if it was in the liver, the mass of growth looks like liver cells
2. Malignant neoplasms- does not move around when touched, attaches to underlying tissue. Anaplastic tissue present- doesn't look like it's forebearers. Could metsthesize

Inability to reverse mitochondrial dysfunction
Cell membrane damage
Ca++ influx
Free radicals

The sum of the degradative reaction occuring after cell death

1. Autolysis
Self-digestion by cells own lysosomal enzymes
After death, all tissues autolyze
2. Heterolysis
Digestion by living white cells

Cytokines act more locally

Graves

ACTH, GH, Prolactin, LH, FSH, TSH, MSH

Vasopressin, Oxytocin

All the time. Pitutary tumor will make it release even more

galactorrhea (flow of milk from the breast) and amenorrhea (loss of menstruation) in women, and impotence and decreased libido in males

headaches, infertility and weight gain in both sexes

Aldosterone, Adrogens, Glucocorticoids

Hypersecretion results in “moon face”, “buffalo hump”, easy bruising (because they interfere with platelet aggregation from TX2 and prostaglanding pathway), acne (body can’t fight off infection), depression

fluid loss with hypotension, hyponatremia( loss of salts), muscle weakness, and skin pigmentation changes (ACTH has a melanocyte stimulating hormone near the nipples)

Hypersecretion results in increased metabolic rate, tremor, heat intolerance, weight loss (diet pills have thyroid hormone). May also have tremor.

Hyposecretion results in decreased metabolic rate, cold intolerance, weight gain

Spermatogenesis in males, stimulates ovarian follicles to grow and produce estrogen in women

Stimulates testosterone synthesis in males, and estrogen and progesterone from the corpus luteum in women (maintain pregnancy in women)

Vasoconstrictor

Promote Reabsorbtion at the level of the kidney

Diabetes insipidus

Hyponatermia (low Na level) and cerebral edema

Oxytocin

Stimulates Uterine Contraction, milke ejection in lactacting women. Causes you to trust.

Increased

10%

Fourth the sixth decade

Benign, but can still cause neurologic problems form physical intrusion

1 cm

EVERYTHING AND ANYTHING!

1. Hyperprolactinemia(most common): amenorrhea, galactorrhea, impotence
2. ACTH: Cushing’s disease
3. Growth hormone: acromegaly

When the tumor becomes a macroadenoma

Compression and movement into the cavernous sinus

Bitemporal Hemianopsia. Usually beging in superior temporal field

Headaches early in the morning.
Weight gain.
Loss of sexual drive.

CT and MRI with Gadolineum enhancement

Pharacological intervention in the hopes resolution

Transphenoidal surger

60%

Prevent decrease of hypothalamic dopamine, which is a check for prolactin levels. Thus, Loss of dopamine function will increase prolactin levels. Drugs could also interfere. MOI and cimetidine are examples

Dopamine agonists

1. Bromocriptine- Three times a day, orally or vaginally. Associated with tumor regression
2. Cabergoline- Twice weakly orally or vaginally.

Bromocriptine is cheaper however has lower patient compliance because it must be taken twice to three times per day
Cabergoline is more expensive, however, it only has to be taken twice weekly

Excessive GH in adults- acromegaly
Results in growth in the soft tissues, bone

Enlargement of the jaw with separation of the teeth
Hand and feet enlargement
Osteoarthritis
Entrapment neuropathies (carpal tunnel)
Abnormal glucose tolerance- Body needs energy. Brings on diabetes melitus. Makes tissues resistant to insulin as well
Heart failure (HF)

Batman: the Dark Knight

Transphenoidal surgery
Radiotherapy 3-10 normalization time
Pharmacological intervention

Both are Somatostatin Analogues
1. Ocreotide- given q8h SubQ. If effective, switch to injectable suspension q4w
2. Lanredotide- May be possible to give injection q6-8 wks

Bromocriptine and Cabergoline. Could shrink tumor.

Pegvisomatnt,

When somatostatin and surgery does not work by themselves

Cushing's syndrome

Exogenous introduction of steroids. usually not created with topical steroids

Cushings syndrome is ALWAYS elevated levels of steroid in the body. Cushings disease is whenever that elevated level of steroid is from a pituitary tumor

50%

5 times

Third to fourth decade

Syndrome

Independent

15-30%

Neoplasm

A neoplasm, usually in the lung, that secretes ACTH.

No

15%

Early:
Gradual weight gain
Hypertension

Later: Truncal obesity
Moon face
Buffalo hump
Muscle weakness (can't climb stairs)
Hyperglycemia- 20% of patients have Diabtets
Thinning of skin
Osteoprosis
Depression
Increased infection
Hirutism- Body hair
cataracts

Dexamethasone suppression test. Most of the time, the tumor in the pituitary will still respond a little to the hypothalamus. If you give a massive steroid, the hypothalamus will put the breaks on ACTH. This will lower endogenous steroid. It the tumor is elsewhere (lung) endogenous steroid levels will not increase

Transphenoidal surgery

Removal of the adrenal gland, leaves patient with Addison's disease.

Rapid tumor growth (nelson's syndrome)

No

Aldosterone secreting adenoma of the adrenal gland. 60-80% of primary hyperaldosteronism cases are this.

Hypertension due to increase sodium and hypokalemia to to potassium insufficiency.

Tetany- inability to contract muscles
Parasthesia- Inability for muscles to contract

Women/men in a ration of 2/1

Anything other than a tumor. Usually poor output. Body then ramps up Renin-angiotensins system to compensate.

1. Patient with chronic insufficiency having a massively stressful event
2. Sudden witdrawal from exogenous steroids after patient's adrenal has atrophied- patients should be taper off to reduce this possibility

Progressive destruction of the adrenal cortex

Autoimmune, Tuberculosis, and metastic neoplasms

1. GI disturbances
2. Hypotension (secondary to loss of aldosterone)
3. hyperpigmentation- Too much melanocyte stimulating hormone
4. Weakness

Medulla is the neurologic tissue that is at the center of the adrenal cortex

Chromaffin cells- secrete and synthesize epinephrine

Tumor of the adrenal medulla which gives rise to massive sympathetic discharge- symptoms include everything you would think of with such a burst

10% malignant
10% bilateral
10% tisue outside adrenal
10% in Children
10% runs familialy
10% recur
10% present with stroke

Stroke from myocardial ischemia (heart beats so fast it can't supply itself with blood). Leads to renal failure in kidney

Thyroid Eye disease

Thyroglobulin- precursor to thyroid hormone

Body makes 20 times more T4, however T3 is 5 times more biologically active

Bound to Thyroid binding globulin (TBG). It stays this way till the body needs it

Up-regulates carbohydrate metabolism, lipid metabolism, and increases protein synthesis which results in a net increase of the metabolic rate

Any time! You are most likely to get it during a hypothyroid state from the glands attempt to become hyperplasic or hypertrophic to compensate for lack of hormone. You can get goiter during Euthyroid and hyperthyroid state.

Thyrotoxicosis

1. Graves- Most common
2. Ingestion of too much thyroid
3. Hyperfunctional multinodular goider
4. pituitary adenoma very rare (you can get thyroid tumor, but it usually causes nothin)

1. INcreased metabolism
2. Nervousness, irritability
3. Tachycardia- Most common symptom
4. Hypermotility of gut- leads to dehydration
5. Staring + lid retraction
6. Heat intolerance
7. Insomnia
8. Scanty menstrual periods

0.4-1%

20-40 years

7:1

HLA-DR3

Very low, because the the hypothalamus does not want any more thyroid even though there is a massive amount in circulation

1.Thyrotoxicosis
2. Opthalmopathy In 40-50% Exopthalmos from swelling of EOM (patient could be seeing double). Lid retraction, edema, keratitis and compressive optic neuropathy
3. Pretibial Myxedema- Thickening of tissue under the skin in the lower legs

Propanolol

Inhibit the oxidation of iodine and thus decrease thyroid hormone synthesis

1. Propyhthiouracil- one pill everyday. Acts faster and is one third the price of methimazole
2. Methimazole- same dosage of propylthiouracil.

Continue for 1-1.5 years with tapered does in hopes that patient becomes Euthyroid (aka stop producing thyroid stimulating immunoglobuline)

1. Remission less than 20%
2. Side effects- Rash and joint pain, Agranulocytosis (don't produce Granulocytes- EVER AGAIN)
Hepatitis

Rapid cure and low rate of becoming hypothyroid

Damage to parthyroid gland and damage Laryngeal nerve (you can't talk!)

iodine 131

Reduces thyroid size and function within 6-12 weeks

Cure rate approaches 100%, but most likely patient will become hypothyroid. 70% have become hypothyroid after 10-15 years

Primary hypothyroidism means that the thyroid isn't producing sufficient amounts of hormone. High TSH, low thyroid
Secondary- Thyroid works find, just not being stimulated by the pituitary and hypothalamus

1. Removal of thyroid or radioactive therapy
2. Hashimoto's disease
3. Primary idopathic hypothyroidism- 5% of population has this affliction

Just the opposite of hyperthyroid
Generalized apathy and mental sluggishness
May mimic depression early in disease
Slow speech
Fatigue
Cold intolerance
Obese
Delayed DTR
Decreased bowel motility with resultant constipation
Bradycardia, heart failure

Hypothyroid in children due to lack of iodine in diet or inborn metabolic error. Short stature and CNS impairment. Could occur in Utero

June 13, 1984

Immune destruction of TSH receptors on the thyroid gland

HLA-DR5

15:1

Transient hyperthyroidism that is followed up by the profound hypothyroidism that is hashimoto's disease

L-Thyroxine qd. May be possible for weekly adminitstration

Nodules that take up radioactive iodine are benign
Nodules in younger patients are more likely to be neoplastic
Nodules in males are more likely to be neoplastic

Surgical removal

- Chvostek’s sign: Tap on facial nerve in front of ear causes contraction of facial muscles and upper lip
-Trousseau’s sign: Inflation of BP cuff for 3 minutes causes carpal spasm (MCP flexion with PIP (proximal interphalangeal) and DIP (distal interphalangeal) extension and adduction of thumb). Cerebral Palsy like thing in the hand.

Insuline resistance syndrome

5X DM
3X Cerebrovascular

Central body weight obesity
Insuling resistance
Lipid abnormalities- Lipid abnormalities
Triglycerides > 150mg/dL
Low HDL: M < 40 mg/dL, and W < 50 mg/dL
Elevated BP- >130/85 mmHg

5-10

160/100000. Mostly children

HLA-DR: 3 or 4 for Caucasians, 7 for African descent, 9 for Japanese)

LADA- Latent autoimmune Diabetes in Adults. Usually adults over the age of 35

Slowly progressive form of type I DM

Glutamaic acid Decarboxylase

Sulfonylureas

Prevalence is ≈ 6,670 per 100,000 population

IL-6 and CRP

80

Because the body can't take glucose into the cells, so it thinks that it is starving. So it releases glucose from the liver.

1. Decreased uptake of glucose
2. Decreased receptors on cells
3. decreased activity of peroxisome proliferator-activated receptors (PPAR) that controls the entry of sugar and fat into cell’s nucleus.
4. Excessive protein production in the PTPN1 gene
5. Deficiency in osteocalcin

More of a blending of the type diabetes. They are an obese patient presents with positive antibodies against their Beta cells. Sometimes referred to as LADA which is incorrect. LADA are thin

Must have a family member who developped it before the age of 30

Single gene.
6 variants

Low dose insulin, diet, or oral drugs

Type II

after delivery

insulin

yes

1. Polyuria
2. Polydipsia
3. Fatigue
4. Possible weight loss
5. Infections from decreased WBC activity and great media for bacteria in the blood

180mg/dL

ketones

Ketonemia, ketouria, and ketoacidosis (pH of blood drops beneath 7.2)

greater than 200 mg/dl

Greater than 126 mg/dl

Portions of blood glucose are bound to hemoglobin, making the amount of testable glucose in the blood 15% of plasma

False. Many times it is the tissues that don't need glucose that are damaged

Type I 30-50% (Major cause of death)
Type II 6-9%

ACE inhibitors

Microalbuninuria (trace amounts of alubin in the urine)

blood vessals

Heart disease

Some one who has already had a myocardial infarction

1. Claudication (limping)
2. Skin ulcers from poor circulation
3. Gangrene

50%

4 Times

A. Leg pain relieved by rest
B. Cold feet with reduced or absent pulses
C. Nocturnal leg pain relieved by dangling legs over side of bed or walking
D. Loss of hair on the foot and toes

50%

Schwanns cells

1. Paresthesias (pins and needles)
2. Decreased vibration sense
3. Decreased DTR (deep tendon reflex)
4. Slower conduction velocity

They can't feel ulcers growing on the bottom of their feet

1. Flucuation in vision
2. Retinopathy caused by new, leaky blood vessals
3. Glaucoma
4. Heart failure signs from fundus exam
5. Cataracts

non-enzymatic binding of glucose to proteins in body tissue. It is a function of how much plasma glucose you have. more glucose, more glycosylated end products