Uploaded by Ethan Lazare

Semerster 2B block 1 review

advertisement
Semester 2B block 1 review
Histology
Histology of skin
7 functions of skin?
3 layers of skin? What type of cell/tissue is found in each?
4 (or 5) layers of epidermis? What secondary cells are found in the layers?
2 layers of the dermis? What type of cells is found in each? What type of tissue?
What is the 5th cell layer only found in thick skin?
What are the 2 types of skin? What differs in the location, layers, receptors, hair follicles and glands of
these types of skin?
What is the function of melanocytes and where are they found?
What are the 3 types of projections of the layers of the epidermis outwards, epidermis inwards and
dermis outwards respectively?
What are the types of sensory receptors found in skin (5 mentioned, 3 more important than the rest)?
Where are the 3 corpuscle types found? What do they sense?
What type of gland structure do sebaceous glands have? describe them histologically, secretion type?
What type of gland structure do eccrine sweat glands have? describe them histologically, secretion
type?
What type of gland structure do apocrine sweat glands have? describe them histologically, secretion
type?
Histology of cartilage and bonel4
What functions does cartilage serve?
What are the 2 main ECM components of hyaline cartilage?
How is cartilage supplied with nutrients?
What makes up most of the volume of cartilage?
What 3 cell types are most prevalent in cartilage?
What are the 2 perichondral layers and what cells are they made of?
What type of growth happens from the perichondrium?
What type of growth happens in the cartilage itself?
What is the name of the gap where chondrocytes are found and what is the name for a group of
chondrocytes?
What is the name for the two types of matrices found within cartilage?
What are the 3 types of cartilage? What distinguishes each of the types?
Where are each of the 3 types of cartilage found?
What are the 2 types of specialized hyaline cartilage? What makes them special?
What are the 2 bone/calcium regulation hormones?
What mineral is bone made of?
What are the 2 types of ossification?
What is a spicule? What are a trabeculae?
What do osteoblasts secrete?
Where are osteoblasts/osteoprogenitors found?
What type of cell shape do osteoblasts and osteoprogenitors have respectively?
What is a lacunae?
What are canaliculae?
What are osteons?
What are cells resorb bone and what cells do they come from?
What differs in immature and mature bone?
What are the 2 types of bone found in long bones? What differs between them?
What are found within haversian canals?
What is paget disease?
What is the epiphysis and diaphysis?
What are the 2 layers of periosteum? What are they made of and what is their functions?
What is found in endosteum?
What type of ossification is used by long bones?
What type of ossification is used in the skull?
What is the name for the area where ossification of long bones begins?
What differs in adult and child long bones?
Name the 5 zones of bone formation?
What are the 4 steps in bone repair after a fracture?
Anatomy
Intro to Musculoskeletal system
8 regions of the body?
10 regions of the lower limbs?
3 planes of the body?
Anatomical motions of the joints?
4 tissue types of the body?
3 layers of the skin?
3 layers of fascia?
Components of neurovascular bundles?
3 types of muscle? Voluntary/involuntary? Striated? Location?
3 layers of fascia within/around muscle and their tissue types?
Levels of division of muscles?
What is an origin?
What is an insertion?
What is the belly of a muscle?
What is a tendon? What is an aponeurosis?
What are the 6 types of bones and give examples for each?
2 types of ossification?
2 types of bones in long bones?
Describe the head of a bone?
Describe a crest of a bone?
Describe the condyle of a bone?
Describe the epicondyle of a bone?
Describe the tubercle, tuberosity and trochanter respectively?
Describe a foramen of a bone?
Describe the fossa of a bone?
What differs in ligaments and tendons?
What is a fibrous joint?
What is a syndesmosis?
What is a gomphosis?
What is a synchondrosis?
What is a symphysis?
What are the 6 subtypes of synovial joints and list one example of each?
Anatomy and development of the skin and subcutaneous tissue
What key steps happen in the first week of development?
What 3 steps take place in the second week of development?
What key steps take place in week 3 of development?
What forms the epithelium of skin?
What forms the CNS?
What forms the PNS?
What forms the dermis/skeletal muscle of the back and bones of the back/cranium?
What forms the urogenital system?
What forms the rest of the dermis (except the back) and skeletal muscles/bones of the body(except the
back)?
What forms the organs except the urogenital system?
What forms the lining of the GI and respiratory tract?
What are the 5 layers of the epidermis? (2 names for the innermost layer)
What is ichthyosis? What is the more specific condition involving newborns?
Where are melanocytes found? Function?
Where are merkel cells found? Function?
Where are Langerhans cells found? Function?
What is polythelia?
What is polymastia?
What is an accessory nipple?
What is an inverted nipple?
Anatomy of the axial skeleton
What part of the spine are concave and convex respectively?
How many bones are there of the vertebral column? How many for each section?
What is the spinous process?
What are the articular processes?
What are the transverse processes?
What is the body of the spine?
What are the lamina of the vertebrae?
What are pedicles of vertebrae?
What 2 structures form the facet joints of the vertebrae?
Where do nerves exit the vertebral canal?
What is the name of the ligament that connect spinous processes?
What is the name of the ligaments within the vertebral canal?
What is the ligament found just in front of the body of vertebrae?
What is the ligament found just behind the body of the vertebrae?
What is the name of the ligament found between transverse processes?
What lordosis and kyphosis respectively?
What side (left or right) would the spine curve in a right-handed individual? Left-handed?
What motion does the atlanto-occipital joint allow?
What makes the C1 vertebra unique?
What type of motion does the atlanto-axial joint allow?
What makes the C2 vertebra unique?
What is the defining feature of all cervical vertebrae?
What makes the C7 vertebra unique?
What are the 2 most important neck bone breaks (name and bone)? Why is one worse than the other?
What is the defining feature of the thoracic vertebrae?
Which ribs attach only at one costal facet?
What is the name for the facet on the transverse process?
What is the defining feature of the lumbar vertebrae?
What is abnormal about the L5 vertebra?
What are the 2 parts of the intervertebral disks?
What number of true, false and floating ribs are there?
To which vertebra(e) would the 1st rib attach?
To which vertebra(e) would the 3rd rib attach?
To which vertebra(e) would the 10th rib attach?
What is the manubrium?
What is the purpose of the costal groove?
What are the names of the 2 costal facets?
What is the name for the rib/vertebra joint?
What is the name of the shoulder joint?
What is the name of the joint where the collarbone meets the shoulder blade?
What differs in the form and function of the shoulder and hip joints?
What are the names of the 5 superficial/extrinsic back muscles?
What is the function of the 5 superficial/extrinsic back muscles (each individually)?
What is the only back muscle innervated by a cranial nerve? What is the nerve?
What innervates all superficial/extrinsic back muscles except the trapezius?
What 3 muscles form the triangle of auscultation?
What are the 4 intermediate back muscles?
What is the function of each of the 4 intermediate back muscles?
What innervates the 4 intermediate back muscles?
What are the 5 deep/intrinsic back muscle groups?
What are the functions of the 5 deep/intrinsic back muscles?
What is the general function of the superficial/extrinsic back muscles as a group?
What is the general function of the intermediate back muscles as a group?
What is the general function of the deep/intrinsic back muscles as a group?
What are the 2 pectoral groups and what is their function?
What is the function of the anterior serratus groups?
Medical Microbiology
Bacterial skin infections
Cellulitis?
-Acute inflammation of subcutaneous tissue, commonly caused by S. aureus
-rapid edema, redness and heat (with 24-48h of minor injury)
-many syndromes begin with cellulitis;
Erysipelas?
Distinctive type of cellulitis caused by S. pyogenes
-infection of dermis with lymphatic involvement
-raised, clear demarcated, salmon-red or “fiery red” colour
-often unilateral, sometimes bilateral
-fever, chills, pain, leukocytosis
-specific virulence factors – Not mentioned
-may follow throat(children) or infection/trauma/surgery (adults);
Group A Strep (S. pyogenes)?
Gram positive cocci in chains
-Coagulase negative(like all strep)
-Lancefield group A
-Beta-hemolytic
-Bacitracin sensitive
Virulence factors
-M-proteins (M1 or M3)
-hyaloronic acid capsule
Enzymatic toxins
-Hyaloronidase – spreading factor
-Streptodornase – breaks DNA and liquifies pus
-Streptokinase – fibrolysin
Causes:
-Erysepelas
-Scarlet fever/Scarletina
-Rheumatic fever
-Post strep glomerulonephritis
-Pyoderma
-Impetigo – (S. aureus is more likely without culture);
Scarlet fever?
Caused by infection with S. aureus lysogenized with Spe genes (superantigen)
-triggered by delayed type hypersensitivity
-toxins are “erythrogenic”
-causes maculopapular rash with “sand paper texture”
-rash blanches with pressure – “Schultz-Charleton phenomenon”
-“Pastia lines” – rash darker in skin folds
-“strawberry tongue”
-fever
begins several days after strep pharyngitis or rarely surgery/trauma;
Acute post streptococcal glomerulonephritis?
Immune complex mediated (type 3) hypersensitivity to S. Pyogenes
-glomerulonephritis
-blood in urine
-foamy urine
-swelling(edema) of the face
-hypertension;
Acute Rheumatic fever
Inflammatory changes in heart(carditis), joints(arthritis), blood vessels and subcutaneous tissues caused
by S. pyogenes infection
-First attack usually in those 5-20yo
- “Jones criteria” used to diagnose
-preventable if treated within 10 days of infection
-symptoms begin 2-3 wees post pharyngitis or 3-6 weeks post skin infection
-type 2 Hypersensitivity caused by cross-reactivity;
Pyoderma?
Localized postules(or vesicles) filled with pus caused by S. pyogenes
-similar to folliculitis but may or may not be associated with hair follicles;
Impetigo
Vesicular/postular bacterial skin infection caused by S. aureus or S. pyogenes (more often S. aureus)
-often transmitted by school children
-highly contagious, requires break in skin
-lacks fever or sepsis
-secondary spread through scratching
-prevalent during warm, moist weather
-superficial erosion and crusted lesions
-bullous and non-bullous forms
-self limited, but better off treated by topical/oral antibiotics;
Staph aureus?
Gram positive cocci in clusters
-coagulase positive
-catalase positive (unlike S. pyogenes)
-oxidase negative
-mannitol fermenter (unlike other staph)
-Fibrolysin
-Beta hemolytic
-about 20% carriers in general population
Virulence factors – streptolysin – enzymatic toxin(oxygen stable hemolysin);
Bartonella henselae?
Facultative, intracellular gram negative rod
-The causative agent of cat scratch fever and bacillary angiomatosis(immunocompromised
-spread by animal scratches
-small papule develops 5-10 days after bite or scratch
-virulence factors – None known
-zoonotic – many animals but especially cats(>40%)
-severe lymphadenopathy progresses to
-immune limited sever swelling of axillary lymph nodes(cat scratch disease)
-progresses to bacillary angiomatosis(systemic) in immunocompromised;
Cat scratch disease?
Caused by bartonella henselae in immunocompetent individuals
-immune limited to extreme swelling in cervical/axillary lymph nodes
-small papule develops 5-10 days after scratch/bite
-progresses to pustules at site, may last several weeks;
Bacillary Angiomatosis?
Progression of Cat scratch disease (caused by Bartonella henselae) in immunocompromised
-proliferative, neovascular, cutaneous and visceral lesions
-red/purplish elevated nodular lesions(satellite lesions common)
-May resemble cherry angiomas or Kaposi sarcoma
-May ulcerate and produce serous drainage with or without visible blood
-closer/histological inspection reveals lobular proliferations of small blood vessels
-triggers cytokine production
-hepatosplenomegaly due to visceral lesions of these organs;
-silver shows a few short rods in the central necrosis
-treat with prolonged antibiotic use;
Abcess?
localized collection of pus(neutrophils generally) surrounded by inflamed tissue;
Foruncle?
Boil,found at site of hair follicle
- may be due to infected follicle or follow other damage to follicle
-often caused by S. aureus infection;
Carbuncle?
Coalesced boils/foruncles often caused by S. aureus
Pasteurella multocida
Gram negative bacilli(rod), aerobe/facultative anaerobe, bipolar staining
-Cellulitis less than 24h after animal bite
-regional lymph-adenopathy
-fever in about 20% of cases
-soft abscesses and tenosynovitis(tendon inflammation)
-in immune compromised patients, may lead to systemic, heart, bone, CNS and abdominal abcesses
-Zoonotic – oral cavity of healthy mammals
-Capsule and fimbrae/pili
Enzymatic/toxin virulence factors
-PMT – potent mitogen
-ToxA
-ToxA and PMT inhibit DC migration
-non-hemolytic;
Actinomyces israelii
Anaerobic, non spore-forming, branching, filamentous gram positive rod(bacilli)
-presence of “sulfur granules” in pus
-grows whitish to rust brown, “molar tooth” shaped colonies on culture
-often caused by trauma, dental work or surgery
-unidentified virulence factors
-cutaneous oral-cervicofacial abcesses – “actinomycosis”
-painful cellulitis
-Dense, hard, fibrotic lesions giving “woody or lumpy jaw”
-lesions may open to surface, releasing pus
-may form granuloma over time if not treated
-may have hemtogenous spread to other tissues(abdomen, thighs, bone, lungs etc);
Mycetoma
Granuloma caused by fungi or Actinomyces israelii;
Viral infections
Measles?
Rubeola virus of the Parmyxoviridae family, negative sense ssRNA enveloped virus
-H(hemagglutinin) spike
-F(fusion) spike – leads to syncytia formation(multinucleated cells)
-Maculopapular rash with fever (101°F/38.3°C)
-cough, coryza and conjunctivitis with photophobia (the 3 C’s)
-Koplik’s spots on buccal mucosa and throat(small blue-white- to grey spots on erythematous base)
-rash associated with CTL cells attacking infected endothelial cells
-infectious 5 days before symptoms and 4 days before rash
-MMR vaccine – live attenuated vaccine;
Complications:
-Secondary bacterial infections
-Pneumonia
-Meningitis/encephalitis
-Severe Schlerosing Panencephalitis develops 1-10 years post infection, progressive usually fatal CNS
disease that leads to mental/physical impairment in those who survive – more common in those
under 2yo;
Rubella Virus?
Cause of rubella aka german measles aka three day measles, ss, positive sense linear RNA enveloped
virus
-H-glycoprotein spike but no F peplomer
-Maculopapular rash associated with immune complex formation
-does not result in syncytia formation
-teratogenic in fetal infections
- low fever
-rare mild coryza and conjunctivitis
-resembles mild case of rubeola
-incubation about 7-14 days, lasts 3 days;
Congenital rubella?
Cause of rubella aka german measles aka three day measles, ss, positive sense linear RNA enveloped
virus in newborn baby
-Tranplacental transmission
-acts as teratogen – patent/primary ductus arteriosus, cataracts, glaucoma, blindness, mental
retardation and deafness
-“blueberry muffin baby” – newborn with multiple purpura;;
Erythema infectiosum aka Fifth disease?
Caused by parvovirus B19, naked ss linear DNA(+ or -)
-Maculopapular rash with immune complex formation
-results in inactivation of erythroid precursor cells leads to drop in hematocrit
-“slapped cheek” syndrome
-lacy, reticulate maculopapular body rash appearing on trunk, limbs and soles of feet
-Aplastic anemia in those with underlying anemias(sickle cell etc)
-fatal hemolytic anemia in patients with previous aplastic crises)
-Hydrops fatalis in cases of rare transplacental infections
-Tropism for erythroid precursors via P-globoside antigen
-+ or – for pronormoblasts in blood smears;
Exanthem subitem aka roseola?
Caused by HHV-6, linear dsDNA, enveloped virus
-replicates in T-cells, B-cells and oropharyngeal epithelium
-life long latency in humans
-confirmed by IgG pair sera or IgM
-maculopapular rash
-fever ends then rose colored maculr to maculopapular rash on trunk, it could be absent in the face and
legs
-3 to 5 day history of high fever(103°F or 39.4°C)
-occasional mild upper respiratory symptoms
-in some infants may be fever without rash
-infantile fever may contribute to seizures;
Chickenpox?
Caused by herpes varicella-zoster virus (enveloped linear dsDNA) in children
-Vesicular rash with viral replication in the epidermis
-cytopathology leads to tissue damage in the epidermis
-“dew drop on rose petals” or vesicular rash with erythematous background
-progresses from papule to vesicle to scab, with all stages present(asynchronous lesions);
Perinatal varicella zoster?
Severe disease caused by mother infection between 5 days prior and 2 days post birth
-severe due to limited mother antibodies
-same symptoms as chickenpox, more severe;
Shingles?
-latent recurrence of Varicella zoster in previously infected individuals
-painful vesicular lesions follow dermatomes and are unilateral
-may be treated with antiviral and can be prevented with live attenuated vaccine
-may lead to bacterial necrotizing fasciitis as secondary infection;
Herpes simplex virus?
(linear dsDNA enveloped virus)
-causes cold sores(HSV1) and genital herpes(HSV2)
-irritable vesicular lesions, with latency in trigeminal ganglia
-common;
Hand, foot mouth disease?
Coxsackie virus, in picornaviridae family, positive sense ssRNA, no envelope
-vesicular eruptions on the hands, feet and palate
-usually children under 10, may spread to older adults
-fever, sore mouth/throat, anorexia
-meningitis rarely
-children will not even eat their favorite foods;
Papillomavirus?
-HPV, non-enveloped dsDNA viru
-may lead to cervical, oral and laryngeal cancer/warts
-pap smear;
Moluscum contagiosum?
Pox-viridae dsDNA enveloped, replicates in the cytoplasm
-Direct contact: contact sports, sexual transmission or contaminated fomites
-Henderson-paterson bodies
-usually self limiting, treatment may shorten duration
-persists from 6 months to 2 years;
Subcutaneous infections
Toxigenic rashes?
Include:
-Scalded skin syndrome
-Staphlococcal toxic shock
-Streptococcal toxic shock
Toxins produced by microbes are transported by blood/bodily fluids and trigger immune response,
resulting in visible cutaneous rash;
Scalded skin syndrome?
Aka “Ritter disease”
-exfoliative toxin binds to cell membrane ganglioside 4, leading to enzymatic degradation of desmoglein1
-rare in those over age 5
-occurs in adults with underlying skin diseases
-Large bullae or blisters erupt in entire body within 48 hours – Nikolsky sign
-Desquamation of epithelium, returns to normal within 7-10 days, with no scarring
-fever;
Staphlococcal toxic shock syndrome?
Primarily “endogenous” infection by toxin(superantigen) producing strains of S. aureus
-toxin gene found on lysogenized phage or plasmid
-can be menstrual (diva cup/tampon) or skin infection, respiratory or osteomyelitis
-caused by superantigen – toxins released into bloodstream.
-“rash resembling sunburn”
-pain is rare- unlike S pyogenes infection
Streptococcal toxic shock?
-primarily an “exogenous” infection of S. pyogenes with SpeA superantigen
-often due to septicemia caused by dirty needle
-septicemia
-toxin produced
-Fever, chills, malaise, nausea, vomiting, diarrhea, shock and even organ failure
-localized erythema – cellulitis
-severe pain is common – unlike S. aureus
-Virulence factors M protein, exotoxin A (speA) present
-hyalorinic acid capsule
-Streptolysins present;
Rocky mountain spotted fever?
Caused by Rickettsia rickettsia(obligate intracellular bacteria) caused by tick bites
-poor gram staining
-reservoir wild animals
-infects endothelial lining of small arteries, veins and capillaries
-leads to hemorrhagic or petechial rash
-start treatment (doxycycline) without confirmation
-2-14 incubation
-fever, headache, maculopapular to petechial rash
-inflammation and vasculitis
-ankles and wrist first to swell then trunk, palms, soles and face
-may become gangrenous;
Lyme disease?
Caused by a Borrelia burgdorferi(spirochetes)
-spread by arthropods
-reservoir wild animals
-“bull’s eye rash”
-progresses to carditis, meningism, bells palsy, polyarthralgias;
Cutaneous Leishmania?
-2 causative agents – L. tropica from South American and L. donavani from Europe/Asia
-Sand fly is the major vector
-relatively painless ulcer surrounded by induration, heals even untreated but leaves severe scar
-may progress to mucocutaneous form, destroying nasal septum and buccal cavity
-worse for immunocompromised
-death from secondary infecton
Mucocutaneous Leishmania?
-can be caused by cutaneous version (L. tropica or L. donavani)
-usually caused by L. brasiliensis;
Visceral Leishmania?
-in south asia
-leads to splenomegaly, infects liver and spleen;
MOTTS?
Stands for mycobacterium other than tuberculosis
-self limiting, rough, wart like lesion
-acid fast, pleomorphic rods, facultative intracellular
--fast growing but low sensitivity;
Mycobacterium leprae?
-obligate intracellular acid fast rods
-Leprosy/ Hansen’s disease/ Neuritis
-Chronic granulomatous infections of the skin, peripheral nerves and upper airways
-prefers low body temperature
-reservoir - armadillos(not proven source)
-transmitted by close contact with respiratory droplets of active cases – not highly contagious
-can be tuberculoid(controlled by Th1) or lepromatous(T-cell deficient or Th2);
Bacillus anthracis?
Gram positive spore forming aerobe
-ubuquitous soil orgaism, also in animals
-calcium dipicolinate spore
-has 3 enzymatic toxins – EF(edema factor), LF(lethal factor) and PA(protective antigen)
-highly associated with people who handle animals and animal products
-EF increases cAMP, decreasing phagocytosis\
-LF is matrix metalloprotease, inactivates MAPKK, tissue necrosis and cytokine production(shock);
Fungal infections
Candidiasis?
Caused by candida albicans a budding/pseudo-hyphal yeast
-generally an opportunistic infection (immunocompromised or loss of normal flora)
-can be cutaneous (diaper rash/folliculitis)
-can be mucocutaneous/oral (thrush)
-onchomycosis – nails
-produces acid proteases and phospholipases
-found in normal flora
-often caused by antibiotic use
Tinea (many forms)?
Caused by dermatophytes (microsporum, trichophyton and Epidermophyton) – monomorphic
septated hyphae
-aka “ringworm” even though fungal cause
-vesicular, or scaling lesion usually with raised border
-appears as concentric rings caused by host reaction to metabolites of keratin degradation
-named according to the location
-corporis(body), pedis(athletes foot), cruris(jock itch), capitis(head), manuum(hands), barbae(beard),
unguium(nails)
-reservoir – humans, soil, animals
-contact sports and other direct contact;
Tinea versicolor?
Chronic mild superficial infection caused by dimorphic fungi Malassezia furfur
-azaleic acid blocks tyrosinase-> depigmentation
-mallasezin induces apoptosis in melanocytes->depigmentation
-lipophilic - associated with oils applied to skin
-culture is not confirmatory
-“spaghetti and meatballs” appearance of yeast and hyphal forms;
Spootrichosis?
Caused by sporothrix schenckii – thermally dimorphic fungi
-“mold in the cold, yeast in the beast”
-cigar shaped yeast at 35-35C
-dark color hyphae at 25C
-cause ulcer to granulomatous lesions that can lead to nodular lymphadenitis
-Risk factor is people working with plants
-florists, arborists, gardeners, outdoor leisure activities;
Pathology
Dermal definitions and clinical history
4 layers of skin?
Epidermis
Dermal-epidermal junction – basement membrane
Dermis
Hypodermis;
0
Download