Path shelf - deck 1 Flashcards
Profound diarrhea, unicellular acid fast creating oocytes. Infectious cysts can be passed in watery stool
Cryptosporidum / HIV, IC
Transmitted via spores, DKA predisposes to infection. Hyphae are non-septated with 90’ degree angle branching. Can cause black eschar and necrosis of nasal cavity/eyes with neuro defects -> death.
Murcor – Rhizopus
DM, IC
Strawberry cervix, cervicitis – burning, itching, malodorous with yellow/green discharge. Diagnosed via wet mount showing motile trophozoits – Treatment Metronidazole
Trichomonas
Sexually Transmitted
Psuedohyphae at 25C, germ at 37C (opp of mold in the cold, yeast in the heat), Catalase +; increased susceptibility in CGD, Diaper rash, inhaler for corticosteroids, KOH prep oral candida, AIDs defining illness MAX CD4 100 -
Candida
IC, CGD, HIV, DM
ssDNA, naked virus (smallest virus). Transmitted via respiratory droplets causing “slap cheek” or 5th disease – starts on face and moves down. Adults – joint pain, arthritis, soreness. En Utero baby can cause hydrops fetalis.
Sickle cell patient can cause aplastic anemia due to shut down of BM.
Thalassemia B Major: Aplastic crisis
Spherocytosis: Can cause aplastic crisis
Parvo B19
Sickle Cell, Hydrops
Spirocytes – can cause lyme disease, erlichosis, bubesiosis. Do not gram stain. Wright/Giemsa used for diagnosis.
Stage 1: Target lesions with Bulls eye rash – chronic migrains, fever, papule -bite
Stage 2: Heart block – myocaridits, bilateral bells palsy
Stage 3: Joint pain, arthritis, migratory arthritis, meningitis, encephalopathy
Treatment: Doxycycline (stage 1), Ceftriaxone
Borrelia Burgdorferi
Tick Exposure
Coughing, macrophages with intracellular oval bodies. Histoplasma much smaller than RBCs. Can cause granulomas which look similar to TB – have calcification of hilar lymph nodes. IC can cause hepatosplenomegaly. KOH used for diagnosis .With nucleus = histoplasma (without = coccid)
Histoplasma
Bird/Bat droppings
IC
Severe hemorrhagic colitis by O157 H7 most commonly from undercooked beef. Symptoms: bloody diarrhea. Does not ferment sorbitol. Shiga like toxin can cause hemolytic uremic syndrome which damages endothelial cells of capillaries and glomerulus -> Thrombocytopenia and platelet clumps
EHEC
Raw Hamburger
Cysts of giardia (flagellated) from feces in unfiltered water – bloating, flactulence, and foul smelling diarrhea (steatorrhea). Deficiency in DEAK due to this. Treatment: Metronidazole
Giardia Travels/Campers unfiltered water
Grows green colonies - Induces M cells in peyers patcheert6 s to phagocytose them and escape. Then use host actin cytoskeleton to create a tail and propel itself from one another. Damages tissues to release cytokines that will watery -> bloody diarrhea. Leads to Hemolytic uremic syndrome in children <10 y/o with acute renal damage and schistocytes. Treatment: Macrolide/Fluoroquinolone.
Shigella
Fecal/Oral
Gram – non-lactose fermenter, motile, H2S positive with black colonies. Undercooked chicken -> inflammatory diarrhea.
Typhi: Typhoid Mary – Harbored in gallbladder, stayed longer in stool with antibiotic use. #1 cause of osteomyelitis
Salmonella Raw chicken OR
Human Source
Osteomyelitis Sickle cell
Ammonium magnesium phosphate stone – Ammonia urease + which makes staghorn calculi to struvite stones causing pain and kidney stones. Symptoms: fishy odor, UTI, pain. H2S +
Proteus
Staghorn Kidney
Attracts neutrophils along with IL-8, C5a
LTB4 Chemotaxis
Underdeveloped 3/4th pharyngeal pouch - Thymic hypoplasia, recurrent infection and hypocalcemia due to decreased parathyroid. LOW T cells.
Digeorge Syndrome:
XLR Male – LOW T cells. Deficiency of CD43 on T lymphocytes and platelets causing eczema, thrombocytopenia – petechiae, recurrent bacterial infections. Increased risk for pneumococcal infections. T cell depletion.
Wiscott Aldrish Syndrome:
6 months old male – recurrent pyogenic bacteria. B cells don’t mature. No ab in the blood. Absent germinal centers due to no plasma cells. Increased infection with Strep, staph, giardia, enteroviruses.
X-Linked Agammaglobulinemia or Brutons:
boy or girl with low levels of B cells. Increased risk of autoimmune diseases – Increased risk for giardia infection.
Common Variable Immunodeficiency:
Most common. Most patients are asymptomatic. Involve GI, urinary, and respiratory. BLOOD transfusions -> anaphylactic reaction
Isolated IgA deficiency:
Defect in humeral/T cell immunity – Hypoplasia of LN and thymus – Risk of bacterial, fungal, and viral infection. NEED A BM TRANSPLANT for survival. 50% have X linked inheritance.
Severe Combined Immunodeficiency:
Mutation of CD40/L leading to low signals and no differentiation – Low to no IL-4/IL-5. Low IgA, IgG, IgE – recurrent pyrogenic infections at mucosal sites
Hyper-IgM Syndrome:
Increased risk of Neisseria infection
C5-9 Deficiency:
Hereditary angioedema (periorbital edema)
C1 inhibitor deficiency
AIRE mutation – failure of central tolerance. Autoimmunity to endocrine glands. Hypoparathyroidism, adrenal failure, chronic candida infections of skin and oral mucosa
Autoimmune Polyendocrine Syndrome
(ALPS) Mutation FAS/L – breakdown in peripheral tolerance. Self reactive lymphocytes -> Cytopenia, lymphadenopathy, hepatosplenomegaly. Can progress to lymphoma
Autoimmune Lymphoproliferative Syndrome
Mutated FOXP3. Thyroiditis, type I DM, Diarrhea, eczema
IPEX
- Increased vascular permeability, pain, vasodilation, bronchoconstriction
- Mediators of pain: Bradykinin, PGE2
Bradykinin – Pain
IL-6 Secreted by Mo. Important mediator of fever and acute phase response. Is capable of crossing BBB and initiating PGE2 causing activation in hypothalamus. Increased production of No in the bone marrow.
IL-6
• Produced by many different lymphocytes in the body. Found in epithelial cells causing increased diapedesis at site of need. Can cause fever and activation of hypothalamus. Also can cause increased sensitivity to pain, vasodilation, and hypotension. Seen most often in shock.
IL-1, TNFa
Transmembrane protein of Toll-like receptor family – activation of NFkB and inflammatory cytokine production for activation of the immune system. It is well known for recognizing lipopolysaccharide of gram – bacteria. LPS bind CD14. Causing binding of TLR4-MD2 protein -> dimerization. LPS recognition causes conformational change of TLR4 receptors results in recruitment of intracellular domains. Causes release of pro-inflammatory cytokine signaling -> IL-1, TNF, IL6.
TLR4
collagen Type 1: Type 2: Type 3: Type 4:
- Type 1: Bones – most common increased in tensile strength
- Type 2: Cartilage
- Type 3: Granulation tissue, embryonic tissue, uterus – stretchy material
- Type 4: Basement membrane
collagen Scar formation steps
• Scar: Granulation tissue causes increased 1) Fibroblasts (Collagen 3), 2) Capillaries (increased nutrients), 3) Myofibroblasts (contraction of wound making scar smaller). Scar formation Type I collagen -> Type III collagen via collagenase requiring Zinc as a cofactor. Stimulation of collagen formation via FGF/VEGF angiogenesis.
collagen delayed wound healing
infection, vitamin C deficiency, Cu (lysl oxidase) deficiency, Zinc deficiency.
collagen hypertrophic scar
Increase in Type 1 collage.
collagen keloid
usually located behind ear in AA, increased Type 3 collagen
Vasodilation, fever (PGE2), inhibits platelet aggregation – produced by vascular endothelium
• Prostaglandin
Vasodilation – produced by vascular endothelium
• Prostacyclin
Inhibits platelet aggregation, vasoconstriction
• Thromboxane A2
Bronchoconstriction, LTB4 attracts neutrophils
• Leukotrienes
rejection = minutes to hours, type II HSR. No accumulation causing kidney cortex damage – pale infarct.
hyperacute
days – 3-4 months (uncommon years rejection
acute rejection
o Cellular: Most common; extensive inflammation with lymphocytes, plasma cells. Responds to steroids.
o Humeral: Kidney cortex damage same as hyperacute. DOES NOT respond to steroids.
rejection = 6months – years, atrophy of blood vessel with endothelial cell hyperplasia. Compromise of lumen. SLOW NARROWING – chicken fat like. SLOW rise of BUN/Creatinine.
chronic rejection
Graph tissue is attacking the host (BM transplant»_space;). Host is going to be immunocompromised. Graph attacks – skin, GI, liver. Liver damage – abdominal pain, jaundice, edema ect. Bilirubin will build up in the liver. Increased AST/ALT with pruritus due to increased bile salts.
graph vs host