Lambert-Eaton syndrome

Autoantibodies to presynaptic Ca channels  ====>
                  decdrease  ACh release =====>
                                 proximal muscle weakness

Muscle weakness starts with extremities and moves UP.

Weakness improves upon activity.

Ass. with small cell lung cancer.

Myastenia gravis

Myasthenia gravis (MG) - autoimmune disorder in which antibodies form against acetylcholine nicotinic postsynaptic receptors at the neuromuscular junction of skeletal 
muscles.

2  forms of Myasthenia gravis:
 ----ocular 
 ----generalized.

 MG is one of the most treatable neurological disorders.

Initial complaint is a  weakness of the specific muscle.

----- ptosis

---- diplopia

-----ass. with thymoma

symptoms worsen with muscle use

Weakness is typically least severe in the morning and worsens as the day progresses

Weakness tends to spread from the ocular to facial to bulbar muscles and then to truncal and limb muscles

The following factors may trigger or worsen exacerbations:

• Menstruation
• Immunization
• Surgery
• Emotional stress
• Bright sunlight
• Intercurrent illness ( viral infection)
• Medication (eg, aminoglycosides, ciprofloxacin, chloroquine, procaine, lithium, phenytoin, beta-blockers, procainamide, statins)
  
  

  Management

  Therapy for MG includes the following:

  • Anticholinesterase (AchE) inhibitors
  • Immunomodulating agents
  • Intravenous immune globulin (IVIg)
  • Plasmapheresis
  • Thymectomy

  AchE inhibitors

  • Initial treatment for mild MG
  • Pyridostigmine is used for maintenance therapy^{[6, 7]}
  • Neostigmine is generally used only when pyridostigmine is unavailable
  • Corticosteroid therapy provides a short-term benefit
  • Azathioprine, usually after a dose of corticosteroids, is the mainstay of therapy for difficult cases
  • Cyclosporine A and occasionally methotrexate and cyclophosphamide are used for severe cases

Polymyositis

----progressive symmetrical muscle weakness --- painless
---- gradually develop (3-5 months)
---- CD8+ T-cell -induced injury to myofibers
---- SHOULDERS  - most commonly involved

---- loss of muscle mass
---- multiple muscles are involved
---- dysphagia and aspiration
---- cardiac involvement
---- pelvic girdle involvement
---- because this is a systemic disiease:

• Morning stiffness
• Fatigue
• Anorexia
• Fever
• Weight loss
  
  
  
  
  Drug-induced myopathy may result from the following:

  • Alcohol
  • Antimalarials
  • Clofibrate
  • Colchicine
  • Ketoconazole and other azole antifungal agents
  • Statin/3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitors
  • D-penicillamine
  • Vincristine
  • Zidovudine (AZT)

Fibromyalgia

--- women
--- 30-50 years
--- widspread stiffness and musculoskeletal pain

--- paresthesia
--- poor sleep
--- fatigue

Polymyalgia Rheumatica

Pain, morning stiffness in:
--- shoulders
--- hips
--- neck

age > 50 y

ESR  > 40-50

fever, malaise, weight loss

temporal artheritis

Treat: prednison

Sarcoidosis

--- noncaseating granuloma
--- elevated serum ACE level
--- restrictive lung disease
--- bilateral hilar lymphadenopathy
--- erythema nodosum

--- Bell's palsy
---  epithelial granuloma
--- uveaparothitis
--- HYPER Ca


Treat:

Systemic Lupus Erythematosus - SLE

---females
---14-45 years
--- fever, fatigue, weight loss
--- malar rash, photosensitivity, discoid lupus

--- pleural effusion, pneumonitis, pulmonary hypertension, interstitial lung disease

--- neurologic disorders

--- oropharyngeal ulcers

--- photosensitivity

--- arthritis

--- hematologic disorder

--- Libman-Sacks endocarditis
sterile vagetations, verrucous, wart-like

--- hilar adenopathy

--- Raynaud's phenomenon

--- nephritic syndrome
--- false-positive on Syphilis test (RPR-VDRL) due to antiphospholipid ABs that cross-react with cardiolipin used in tests.
--- ANA
--- anti-dsDNA (very specific and poor prognosis)
--- anti-Smith ABs (very specific, not prognostic)
--- antihistone antibodies - drug-induced lupus
----

Ankylosing spondilytis

Chronic inflammatory disease of  spine and sacroiliac joints

Stiffness of spine

Uveitis

Aortic regurgitation

Bamboo spine

Psoriatic arthritis

-----------Joint pain, stiffness, psoriasis
------A---Symmetric
-----------------Patchy

Fingers like "sausage" 

"pencil-in-cup" deformity on X-RAY

Seronegative spondyloarthropaties

Thease are artritis without RF--------no anti-IgG antibodies
commonly in MALES
HLA-B27 association

Sjogren's syndrome

Rheumatoid arthritis

Autoimmune, inflammatory disorder.

Affects synovial joints with formation of the pannus --- MCP, PIP.

----Subcutaneous rheumatoid nodules

----Ulnar deviation

----Subluxation

----Baker's  cyst ------under the knee

Females are most commonly involved than males

Type III hypersensitivity reaction

Majority have "  +  " Rheumatoid Factor (anti-IgG antibody)

HLA-DR4

        Classic picture:       

---morning joint stiffness for more than 30 minutes, that improves with use.

---SYMMETRIC joints involvement

---SYSTEMIC symptoms: fever, fatigue, pleuritis, pericarditis

     Treat:

---NSAID

---COX-2 inhibitors

---glucocorticoids

---disease-modifying drugs:

     Methotrexate, 

     Sulphasalazine, 

     Hydroxychloroquine

Osteoarthritis

picture:   Normal join       vs.       osteoarthritis

Occurs due to mechanical wear and tear ========>
---destruction of articular cartilage and subchondral cysts
---sclerosis
---osteophytes (bone spurs)
---eburnation (polished bone)
---Heberden's nodes (DIP)

---Bourchard's nodes (PIP)

Risk Factors:
1) age
2) obesity
3)  joint deformity

Symptoms:

PAIN in weight-bearing joints after prolonged use, that improves by the REST.

Disease is NONinflammatory.

No systemic symptoms.

Gout

Most common in MALES.

Monosodium urate crystals precipitate into joints due to hyperuricemia.

Hyperuricemia might be caused by:
- high cell turnover
- Von Gierke's disease
- decreased excretion of Uric acid due to thiazide diuretics
- Lesch-Nyhan syndrome
- PRPP excess (phosphorybosil pyrophosphate)


Crystals of monosodium sulphate are:
--- NEEDLE shaped
--- negatively birefringent
--- yellow crystals under parallel light
--- blue when perpendicular light

A___Symmetric.

MTP joint of the big toe ------podagra

TOPHUS: external ear, olekranon bursa, Achilles tendon.

Attack is usually after a binge drinking or a large meal consumption


Treat :
acute: indometacin, colchicine.
chronic: allopurinol, febuxostat, probenecid - uricosurics

McCune-Albright syndrome

Classic triad:

1). Polypstotic Fibrous Dysplasia

2). Cafe-au-lait spots

3). Autonomous endocrine hyperfuction (gonadotropin-independent precocious puberty)

Laboratory abnormalities in bone disorders

1). Osteoporosis : Normal labs, there's just low bone mass

2). Osteopetrosis: Normal labs, but there are thickened, dense bones

3). Osteomalacia (adults) & rickets (children): LOW Ca, LOW Phosphate, HIGH PTH. Bones are soft.

4). Osteitis fibrosis cystica: LOW Phospate, HIGH Ca, HIGH ALP, HIGH PTH. Brown tumors

5). Paget's disease: HIGH ALP. Abnormal bone architecture, increased hat size, hearing loss

Vitamin D deficiency in adults

Low Ca level
Low Phosphate
High PTH level

Rotator Cuff Muscles

4  muscles that act to stabilize the shoulder:

1) Supraspinatus ------> aBDuct arm before deltoid (most common injury)

2) Infraspinatus -------> Rotate arm laterally (pitching injury)

3) Teres minor ---------> aDDuct & Rotate arm laterally

4) Subscapularis  -------> aDDuct & Rotate arm medially

Unhappy triad

Most common football injury to the knee.

1) MCL
2) ACL
3) Lateral meniscus

Passive Anterior Drawer sign --------> ACL is torn                                   

Video: how to test Anterior Drawer Sign

Abnormal Passive Abduction ---------> MCL is torn.

Clefts

1st cleft -----> external auditory meatus

2nd  - 4th cleft ----> temporary cervical sinuses

BRANCHIAL    CLEFTS  from  ECTODERM

BRANCHIAL   ARCHES  from MESODERM

BRANCHIAL    POUCHES from  ENDODERM

Bronchial pouch derivatives

1st pouch       middle ear cavity

                       eustachian tube

                        mastoid air cells

2nd pouch      epithelial lining of the palatine tonsil

3rd pouch  --  dorsal wings--   INFERIOR parathyroids

3rd pouch -- ventral wings --- thymus

 

4th pouch -- dorsal wings --- SUPERIOR parathyroid

Abnormal development of 3rd & 4th pouches:  DiGeorge syndrome

MEN 2A:

1) pheochromocytoma (adrenal medulla)

2) parathyroid tumor (3rd & 4th pharyngeal arches) 

3) parafollicular cells (medullary thyroid cancer); 

       

Tongue

Taste innervation:      CN   VII,     IX,     X
Motor innervation:     CN   XII
Pain:  CN V3,    IX,     X 

1st branchial arch --    anterior 2/3 of the tongue

3rd & 4th branchial arch --    posterior 1/3 of the tongue

Parasympathetic receptors

M1 receptors -------------- q

---  CNS

---  enteric NS

M2 receptors ---------- i 

--- decrease HR

--- decrease contractility of atria

M3 receptors   ----------- q

- increase exocrine gland secretion

---increase gut peristalsis

----increase bladder contraction

-- miosis

---bronchoconstriction

---ciliary muscle contruction (accomodation)

Sympathetic receptors

   alpha 1 receptors --------    q

---increase vascular smooth muscle contraction

---increase papillary dilator muscle contraction --- mydriasis

---increase Intestinal & Bladder sphincter muscle contraction

 alpha 2 receptors  ---------    i

-----decrease sympathetic outflow

-----decrease Insulin release

 beta 1 receptors   -----------   s

--- increase HR

--- increase contractility

--- increase renin release

--- increase Lipolysis

 beta 2 receptors ------------   s

-- increase HR

-- increase Contractility

-- increase Lipolysis

-- increase Insulin release

-- decrease Uterine tone

-- vasodilation

-- bronchodilation 

Granulomatous diseases

1) Mycobacterium tuberculosis

2) Histoplasmosis

3) Treponema pallidum (syphilis)

4) M. leprae

5) Bartonella henselae

6) Sarcoidosis

7) Crohn's disease

8) Berylliosis

Free radical injury

Free radical injury makes cells damaged via: 
--- membrane lipid peroxidation,
-- protein modification,
-  DNA breakage.

This damage can be elimanated by:
-----enzymes: catalase, superoxid dismutase, glutation peroxidase
----spontaneous decay
--- antioxidants: A, C, E

Pathologies caused by free radical injury:
---  IRON overload
--acetominophen
--- reperfusion after ANOXIA (after thrombolytic therapy)
--retinopathy of prematurity
-----bronchopulmonary dysplasia
--CCI4 that leads to liver necrosis (fatty changes)

Лечение Шизофрении

Пациенты с шизофренией демонстрируют значительные улучшения в течении заболевания при лечении фолиевой кислотой и вит В12, как показало рандомизированное клиническое исследование. Стандартное совеременное лечение шизофрении воздействует только на позитивные симптомы заболевания ( галлюцинации) и в гораздо меньшей степени на негативные. А поскольку в предыдущих исследованиях было доказано, что дефицит фолиевой кислоты я вляется фактором риска для этого заболевания. то, соответственно, применение этого сапплемента приводит к улучшению симптоматики. Очень обнадеживающие результаты.!!!

Hyper-IgM syndrome

- Defective CD40L on helper T cells = inability to class switch
- severe pyogenic infection early in life
- High IgM
- very low     IgG,      IgA,     IgE
- high susceptibility to infections

Bruton's agammaglobulinemia

- X-linked recessive  inheritance (patients are BOYS)
- defect in BTK gene       --->      tyrosine kinase gene       --->    blocks pro-B-
    cells to form pre-B-cells.
- recurrent bacterial infections after 6 months because of low maternal IgG due to  
   opsonization defect.
- no thymic shadow
labs: 
- N pro-B-cells
- low maturation
- low B-cells
- low IGs all classes

Infections in immunodeficient patients

1) Bacteria
- sepsis------- (organ has no T-cells)
- Encapsulated: Streptococcus, Staphylococcus, Haemophilus, Moraxela------- (organ has no B-cells)
- Pseudomonas,  Staphylococcus -------(organ has no granulocytes)
- Neisseria -------(organ has no complement)

2) Viruses
- CMV, EBV, VZV---------  (organ has no T-cells)
- chronic infections with respiratory/GI viruses -----(organ has no T-cells)
- enteroviral encephalitis, poliovirus---- (organ has no B-cells)

3) Fungi/parasities
- Candida, PCP ----- (organ has no T-cells)
- GI giardiasis-------(organ has no B-cells, IgA)
- Candida, Nocardia, Aspergillus ----(organ has no granulocytes)

B-cells deficiency produces RECURRENT BACTERIAL infections.

T-cell deficiency produces produces fungal and viral infections.

B-cell and T-cell functions

    B-cell functions:
1) Hyperacute organ rejection is mediated by AB.
2) Allergy - Type I hypersensitivity - Ig E
3) Cytotoxic hypersensitivity - IgG - Type II hypersensitivity
4) Immune complex hypersensitivity - IgG - Type III hypersensitivity

    T-cell functions:
1) CD4 T-cells help B-cells make ABs and produce gamma-interferon, that activates macrophages.
2) CD8 T-cells kill virus-infected cell directly.
3) Delayed cell-mediated hypesensitivity - Type IV hypersensitivity
4) Acute organ rejection 
5) Chronic organ rejection 

Order of enzymes that repair the damage.

Glycosylase -----> Endonuclase ----> Lyase ---> DNA polymerase ---> Ligase

Complications of Diabetes Melitus

Peripheral neuropathy is a very common complication of DM 1 and 2.
Its usually associated with poor glycemic control and long-standing disease.

There are 3 most common types of diabetic neuropathy:

1) Mononeuropathies

  Cranial mononeuropathy:
- oculomotor - III
- facial - VII
- optic  - ischemic optic neuropahty

Somatic mononeuropathies:
- median nerve (bilateraly)
- ulnar
- common peroneal


2) Autonomic polyneuropathy

- GI: gastroparesis, constipation
- CV: orthostatic hypotension
- U: overflow incontinence, neurogenic bladder
- Sex: erectile dysfunction, ejaculatory abnormalities

3) Distal symmetric polyneuropathy

- Sensory: tingling, numbness, burning pain, loss of pain, T, vibration, position sensations.
- Motor: weakness, athrophy, weak DTR.

These deficits are usualy bilateral, symmetric, involving feet and hands.

Transmission of Hepatitis B from mother to baby

Vertical transmission of HepB from pregnant woman to fetus occur only if woman has an active form of HepB.
Look for HBeAg marker (presence of that marker indicates high level of replication and infect ivory of HepB virus). If you revealed this marker , it means there is a higher risk of vertical transmission of HepB virus from woman to the fetus.

All newborns from the mothers with active form of HepB virus are passively immunized at birth with HepB immune globulin (HBIG), followed by active immunization with recombinant HBV vaccine.

Diaphragmatic surface of e heart

Inferior wall of the LV, which is supplied by posterior descending artery ( branch of the R coronary artery)

Primary hypothyroidism

Serum TSH is the singe most important test for diagnostic of primary hypothyroidism. 

Severe IgA deficiency predisposes patients to giardiasis.

Nifedipine

Nifedipine is very good choice for patients with bradycardia. It causes peripheral vasodilation, which may results in reflex tachycardia.

Frequent And prolonged kneeling can cause prepatellar bursitis

DIC

---prolonged PTT
--prolonged PT
----thrombocytopenia
----microangiopatic hemolytic anemia
--low fibrinogen
---elevated D-dimer (fibrin split product)
--------low factor V
----low factor VIII

Levodopa and B6

Vitamin B6 should not be taken by people who on a Levodopa therapy.
B6 increases the metabolism of Levodopa and thus decreases its effectiveness. 

Statines, fibrates, fibric acid derivatives

STATINES  +  FIBRATES = high risk of myopathy
STATINES = hepatotoxicity
FIBRIC ACID derivatives  +  BILE acid-binding resins = high risk for cholesterol gallstones

Doxazosin
Prazosin
Terazosin

Are good choice for both BPH and Hypertension

Angiotensin II in the kidney constricts the EFFErent arteriole, thereby it maintains GFR

ACE-inhibitors decreases the amount of circulating Angiotensin II and causes:

- decrease systemic vascular and arteriolar resistance, thereby reducing GFR

Wernicke syndrome

Ophtalmoplegia
Ataxia
Confusion

Usually these symptoms are resolved after a thiamine administration.
Korsakoff syndrome is a complication of Wernicke encephalopathy, and its hallmark is permanent memory loss and confabulation.

Hepatic angiosarcoma

Is associated with arsenic, thorotrast, polyvinyl chloride exposure.
Tumor cells express CD31 - endothelial cell marker

Pineal germinoma

--- precocious puberty in males, caused by beta-hCG production
-----obstructive hydrocephalus caused by aqueduct all compression by the tumor
---perinaud syndrome: paralysis of upward gaze

Severe aortic stenosis AS

Syncope
Angina
Dyspnea
Systolic Ejection Murmur - at the R 2nd Intercostal Space, may radiate to the Carotid.

Common cause - calcification of the aortic valve leaflets.
These changes appear in the 70th.

Aortic Stenosis with bicuspid aortic valves tends to present by the 6th decade of life.

Metaplasia is an adaptive change in response to chronic epithelial irritation.

Non-selective beta-blockers

Propranolol
Timolol
Nadolol

Inhibit the Epinephrine- and norepinephrine- mediated compensatory reaction to hypoglycemia.
They inhibit hepatic gluconeogenesis and peripheral glycogenolysis and lipolysis. For this reason, non-selective beta-blockers should not be used in diabetic patients.

sex hormone-binding globulin - SHBG

Increased sex hormone-binding globulin in men ------> low free testosterone ===> gynecomastia


Decreased sex hormone-binding globulin in men in women -----> hirsutism
Increased sex hormone-binding globulin in women during pregnancy

Gastrinoma

U GI ulceration, abdominal pain, diarrhea

Cholesterol gallstones - Risk Factors

Caucasian race
Female sex hormones (oral contraceptives taking)
Any ileal disease or resection and consequent malabsorption of bile acids
Obesity
Rapid weight loss
Glucose intolerance
Fibrates, octreotide, ceftriaxon taking
Hypomotility of gallbladder (happens during pregnancy, advanced age, fasting, increased level of triglycerides, prolonged total parenteral nutrition)

Tetanus

It's good idea to vaccinate young adults to lower incidence of neonatal tetanus since newborns get protection from mothers who has immunity.

First vaccination is started at 2 months---> 4 months----> 6 months-----> 15m---->>> 18m------> 10 years-----> -----12years, than boosters are required every 10 years to maintain protective level of ABs

First event in the pathogenesis of acute appendicitis

Obstruction of the lumen

What may cause the obstruction?
- fecaliths
- hyperplastic lymphoid follicles
- foreign bodies
- tumors

Typical manifestation of acute appendicitis:
- pain in the right lower quadrant of the belly
- nausea
- vomiting
- diarrhea
- fever

Selection bias

Loss of follow-up

"Walking pneumonia "----- mycoplasma pneumonia

- nagging nonproductive cough
- low-grade fever
- malaise
Mycoplasma requires cholesterol in order to grow on artificial media

Secondary hyperparathyroidism

The common cause of a secondary hyperparathyroidism is chronic renal failure

Labs: -------high PTH, -----high Phosphate, ----low Ca, ------low Calcitriol,

Histological picture of postreptoccocal glomerulonephritis

----enlarged, hypercellular glomeruli on light microscopy
--"lumpy-bumpy" granular deposits of IgG and C3 on immunofluorescence
-----electron-dense deposits on the epithelial side of the basal membrane on electron microscopy

Warfarin

Rifampin, Phenobarbital, Phenytoin are enhancers a of the cytochrome P-450 ===>>>
Concurrent use of warfarin will result in decreased warfarin efficacy.

Cimetidine , Amiodarone, TMP-SMX inhibit warfarin metabolism

Mitochondrial myopathy

---blotchy red muscle fibers on Gomori trichrome stain
-abnormal mitochondria accumulate under sarcolemma of muscle fibers
-- most important types of the mitochondrial myopathies are:
1). Myoclonic epilepsy with ragged red fibers
2). Lever optic neuropathy
3). Mitochondrial encephalopathy with stroke-like episodes and lactic acidosis

These disease are caused by different impairments of mtDNA.
As we remember sperm mitochondria do not pass into the ovum during fertilization, but transmitted only maternal mitochondria to the mitochondria. ====>> these disease have maternal inheritance .

Prolactinoma in males

----"Bitemporal hemianopia
---Impotence
-----inhibited GnRH, LH, FSH

Hereditary angioedema

--- low serum levels of C1 esterase inhibitor

---aut-Dom or acquired (treatment with ACE inhibitors)

--episodes of painless, non-pitting, well-circumscribe edema of the face, neck, lips,tongue, and also internal organs (tracheobrachial tree, GI,)

Do not use ACE inhibitors in patients with hereditary angioedema.

Wegener's granulomatosis

---necrotizing vasculitis of the U and L respiratory tract ( sinusitis, hemoptysis, ulceration. )
---------rapidly progressive glomerulonephritis
----c-ANCA (target neutrophil proteinase 3)

Amiodaron

Doesn't predispose to tornadoes de pointes, but prolongs QT interval.

Adverse effects of protease inhibitors

Indinavir, ritonavir


They are use as a component of HAART (highly active antiretroviral therapy) and never as a mono-therapy because of the fast formation of the resistance to the entire class of drugs.

1) lipodystrophy ( fat deposition on the back and abdomen, but decrease adipose tissue on the extremities); "buffalo hump"

2) hyperglycemia (from increased insulin resistance)

3) inhibition of P-450

There were listed only important side effects for entire class, but every drug from class has its own adverse effect .

Odynophagia

Painful swallowing

Bladder carcinoma

Painless gross hematuria (blood in urine) is the classic presentation of the bladder carcinoma.
The malignant potential of such tumor depends on he involvement of muscular layer of the bladder.

Recurrent meningitis

Deficiency of the complement factors to form the membrane attack complex (C5b-C9) results in recurrent infections by Neisseria.

Long- term compensatory response that helps to maintain COto the volume overload of aortic regurgitation is an Increase in LV preload (LVDV) in association with LV Hpertrophy

Fifth disease

Non-enveloped......single-stranded......DNA
....Parvoviridae....
Parvovirus - B19
Erythema infectosum
Aplastic crisis in sickle cell anemia
Hydrops fetalis

Catecholamine-secreting tumors - important clues

---episodic hypertension
-tachycardia
-----headaches
--diaphoresis
-tremors

Wernicke encephalopathy in alcoholics

Alcoholics or malnourished patients need to be given IV Thiamine before IV Dextrose.
Without IV Thiamine, there might be precipitated a Wernicke encephalopathy.

Acyclovir

To prevent crystalline nephropathy during acyclovir course , aggressive hydration needs to be provided.

Vomiting after first 24 hours of life

Bilious Vomiting after first 24 hours of life is a sign of intestinal obstruction below the second part of duodenum.
Common causes: intestinal stenosis AND atresia.
Jejunal, ileal, colonic atresias are caused by vascular accident in utero.

There was decreased intestinal perfusion which leads to an ischemia of a segment of bowel, and than subsequent narrowing or even obliterating of the lumen.

Common affected intestinal part is ileum.

When occluded a major vessel (SMA), then there is a large area of an intestinal wall necrosis.

Shistocytes ----- Helmet cells

----Fragmented erythrocytes
------Secondary to mechanical trauma from:
microangiopatic hemolytic anemia OR prosthetic cardiac valves

Intravascular Hemolytic Anemia: decrease Haptoglobin, increased Hemoglobin, LDH, bilirubin

Alpha-antitripsyn deficiency

Smoking in patients w/Alpha-antitripsyn deficiency cal lead to developing of panacinar emphysema.

Mitral stenosis

Diastolic rumble
Pre-systolic accentuating
R-S S3 and /or S4 might be present with the end-stage of MS (pulmonary hypertension)

Severity of MS is de terminated by A2- OS interval, the shorter interval , the more severe MS

Hypoglycemia

Loss consciousness due to hypoglycemia -------glucagon I/m
moderate hypoglycemia ------- treat with 15-30g fast acting carbohydrate ( glucose, fruit juice, milk, soft drink, hard candy)

In medical settings ------D50 (50%glucose solution ) IV 3cc/min

Acute mania

Treatment with mood stabilizing agent ----- lithium, valproate, carbamazepine)
+
Atypical antipsychotic ------ olanzapine

Giant cell arteritis. ------- GCA

Most common form of systemic vasculitis in adults, older than 50
Granuloma tours inflammation of the media
Fragmentation of the elastic lamina of the medium and small branches of the carotid artery
Headache
Facial pain
Jaw claudication (difficulty chewing)
Vision loss (ophthalmic artery occlusion)
Increased ESR

To prevent vision loss therapy with prednisone should be started as soon as possible

Neuromuscular hyperexcitability

Hyperactive jaw jerk reflex - light tapping on the chin elicits masseyer musscle spasm- appears following decreasing Ca level < 7. (Most commons cause of outpatient HYPOcalcemia is hypoparathyroidism, which occurs commonly due to prior loss of parathyroid tissue during thyroidectomy.

Enoxaparin

Has been shown to cause significant reduction in death and recurrent myocardial infarction when used in acute treatment of myocardial infarction as compared with unfractionated heparin and enoxaparin binds and activates Antithrombin III

Multiple Myeloma

You might be considering MM, if there is elderly patient w/ the following findings:
1) fatigue
2) constipation (hyperCa)
3) bone pain (back and ribs are most common parts of the body
4) renal failure

Measles virus (Rubeola)

1. paramyxo
2. Kplic spots (red spots with white-blue center)on buccal mucosa
3. Rash spreads from head to toe (also hand and feet)
4. Subacute sclerosing panencephalitis year later
5. Encephalitis
6. Giant cell pneumonia
7. Cough 
8. Coryza
9. Conjuctivitis

MUMPS virus

Paramyxovirus
Parotitis
Orchitis
Meningitis aseptic
Causes infertility after puberty.

Serologic Markers of Hepatitis

Anti-HAVAb (IgM) - active hepatitis A
Anti-HAVAb (IgG) - priror HAV, protects against reinfection

HBsAg - on surface HBV, just Hepatitis B.

Anti-HBsAg - immunity to hepatitis B

HBcAg - core of HBV

Anti-HBcAg - ABs to HBcAg, during window period

Anti-HBcAg (IgM) - acute/recent infection
Anti-HBcAg (IgG)  - chronic disease

HBeAg - active viral replication and high level of transmissibility
Anti-HBeAg - ABs to e Ag, low level of transmissibility

Chronic watery diarrhea in HIV patients

Cryptosporidium spp. (acid-fast cyst in stool CD4<200)

Respiratory infections in HIV patients

1. Interstitial pneumonia (CMV - owl's eye - intranuclear inclusion bodies)
2. Invasive aspergillosis (Aspergillus fumigatus)
3. Pneumonia (Pneumocystis jiroverci) CD4<200
4. Tuberculosis-like disease (Micobacterium avium-intracellulare), CD4<50

Neurologic diseases in HIV patients

1) Dementia
2) Retinitis (CMV), CD4<50
3) Meningitis, encephalitis (Cryptococcus neophormans - yeast w/narrow-based budding & large capsule), CD4<50
4) Abscess (Toxoplasma gondii - ring-enhanced lesions), CD4<100
5) Encephalopathy, PML (JC virus reactivation, demyelination), CD4<200

Oncologic diseases in HIV

1) Kaposi's sarcoma (HHV-8), lymphocytic infiltration on biopsy, most common malignancy in HIV, cutaneous presentation is most common

2) Squamous Cell Carcinoma (HPV) (anus, cervix)

3) Primary CNS Lymphoma (EBV)

4) Hairy Leukoplakia (EBV) (lateral tongue)

5) Non-Hodgkin lymphoma (large cell type) (EBV), oropharynx

Bugs that look like appendicitis, it means they mimic appendicitis

Yersinia Enterocolitica,
Campilobacter jejuni
non-typhoidal Salmonella

Oligodendroglioma

Pheochromocytoma

Food poisoining

1) Salmonella - poultry, meat, eggs
2) Staph. aureus - meat, mayo, custard
3) E.coli - undercooked meat
4) Cl. botulinum - canned food
5) Bacilus cereus - reheated rice
6) Cl. perfringes - reheated meat
7) Vibrio parahaemoliticus, vulnificus - seafood

Normal Flora

Vagina - lactobacilus
Colon - Bacteroides fragilis, E.coli
Dental plaque - Str. mutans
Oropharynx - Viridans strept
Nose - Staph. epidermidis
Skin - Saph. epidermidis