Patho Acne/Psor/Gout/Glau Flashcards
Pathology of Ance, Psoriasis, Gout and Glaucoma
1
Q
Glaucoma
A
- Elevated Intraocular Pressure THAT RESULT IN DAMAGE TO THE OPTIC NERVE OFTEN LEADING TO LOSS OF SIGHT
- LOSS OF VISIONIS PERMANENT
2
Q
Glaucoma Classification
A
- Closed-angle
- Open-angle
- Congenital
3
Q
Closed-Angle Glaucoma
A
- FLUID DRAINAGE FROM THE EYE IS BLOCKED
- THIS FORM CAN PRESENT GRADUALLY OR SUDDENLY
- INVOLVES SEVERE EYE PAIN
- BLURRED VISION
- MID-DIALTED PUPIL
- REDNESS OF THE EYE
- NAUSEA
4
Q
Open-Angle Glaucoma
A
- THE DRAINAGE FROM THE EYE REMAINS OPEN
- DEVELOPS SLOWLY
- NOT ASSOCIATED WITH PAIN
- GRADUAL LOSS OF PERIPHERAL VISION
- CENTRAL VISION LOSS DEVELOPS WITH LOSS OF VISION
- MAJORITY OF THE CASES
5
Q
Congenital Glaucoma (infantile)
A
- CAUSE IS OBSTRUCTION OT AQUEOUS DRAINAGE DUE TO DEVELOPMENTAL ANOMALIES
- 65% OCCUR IN BOYS IN AN X-LINKED RECESSIVE MODE
6
Q
Glaucoma
Risk Factors
A
- FAMILY HISTORY OF THE CONDITION
- HIGH BLOOD PRESSURE
- INCREASE PRESSURE IN THE EYE (OCULAR HYPERTENSION)
- CONGENITAL MALFORMATION
- EAST ASIAN ANCESTRY
- MUTATED GENES
7
Q
Patho
Open-Angle
A
- REDUCED FLOW DUE TO DEGENERATION AND/OR OBSTRUCTION OF THE TRABECULAR MESHWORK
- REDUCTION IN TRABECULAR FLOW CAUSES AN INCREASE IN PRESSURE AS THE CILIARY PROCESS CONTINUES TO PRODUCE AQUEOUS HUMOR
8
Q
Patho
Closed-Angle
A
- THE CHANNEL BETWEEN THE ANTERIOR AND POSTERIOR IS COMPLETELY CLOSED
- CAUSED BY DISPLACEMENT OF THE IRIS AGAINST THE CORNEA
- ACCUMULATION OF AQUEOUS HUMOR CAUSE ACUTE INCREASE IN PRESSURE AND PAIN
9
Q
Effects of increased ocular pressure
A
- INCREASED INTRAOCULAR PRESSURE LEADS TO CUPPED EXCAVATION OF THE OPTIC NERVE HEAD
- THE CORNEA OR SCLERA BULGES AT WEEK POINTS
- OPTIC NERVE ATROPHY WITH LOSS OF AXONS, GLIOSIS AND THICKENING OF THE PIAL SEPTA
- VISION DECLINES WITH LOSS OF NEURONS
10
Q
Gout
Causes
A
GOUT IS DUE TO PERSISTENT ELEVATED LEVELS OF URIC ACID IN THE BLOOD
11
Q
Gout
Underlying causes
A
- GENETIC FACTORS (60%)
- DIET (12%)
- OTHER HEALTH PROBLEMS (COMORBIDITY)
12
Q
Gout
A
- a form of arthritis
- typically at the base joint of the big toe is affected
- may lead to the formation of kidney stones
13
Q
Gout
Characterization
A
- RECURRENT ATTACKS
- RED,TENDER, HOT,
- SWOLLEN AND PAINFUL JOINTS
14
Q
Diet and Gout
A
Associated with foods high in purine
* MEAT
* SEAFOOD
* ALCOHOL
* MUSHROOMS
* BEER YEAST
* SEAWEED
15
Q
Patho of Gout
A
- HIGH BLOOD LEVELS OF URIC ACID CAUSE URIC ACID TO
CRYSTALLIZE - SUCH CRYSTALS THEN DEPOSIT IN JOINTS, TENDONS AND
SURROUNDING TISSUES - SOMETIMES BLOOD URIC ACID LEVELS ARE NORMAL DURING
BLOOD WHILE DEPOSITS ARE FOUND IN THE JOINTS
16
Q
Gout
Two mechanism for High Uric acid
A
- UNDEREXCRETION OF URIC ACID BY THE KIDNEY (90%)
- OVERPRODUCTION OF URIC ACID (10%)
17
Q
Disorder of Purine Metabolism
A
- CRYSTAL OF URIC ACID FORM AS MONOSODIUM URATE
- URATES PRECIPITATE IN TISSUES
- TOPHI MAY BE WALLED OFF BY A RING OF PROTEINS THAT BLOCK OFFINTERACTION OF CRYSTALS WITH CELL
- URATE CRYSTALS MAY LEAK FROM TOPHI UNDER PHYSICAL
STRESS - LEAKED CRYSTALS THEN TRIGGER A LOCAL IMMUNE-MEDIATED INFLAMMATORY REACTION IN MACROPHAGES
18
Q
NLRP3 INFLAMMASOME
PROTEIN COMPLEX
A
- Initiates Inflammation
- recruits Caspase 1 enzyme
19
Q
Caspase 1
A
- Converts pro-interleukin 1B into active IL-1B
- Important for inflammatory cascade
20
Q
Gout
Anatomical changes
A
- SUBDERMAL NODULES MAY FORM: VARY IN SIZE
- TOPHI MAY FORM FROM CRYSTALS OF URIC ACID SURROUNDED BY CELLULAR ELEMENTS – OFTEN HISTOCYTES
21
Q
Leakage of Crystals from Tophi
A
- bone erosion
- cartilage damage
22
Q
Chronic kidney disease and Gout
A
- NEPHRON FAILS TO FILTER OUT URIC ACID WASTE
- SUCH FAILURE LEADS TO A BUILD UP OF URIC ACID IN THE BODY
23
Q
Gout cause Kidney failure
A
- HIGH BLOOD URIC ACID CAN PRODUCE A KIDNEY FILTRATE HIGH IN URIC ACID.
- SUCH URATE MAY PRECIPATE IN THE RENAL TUBULE AND PHYSICALLY DAMAGE THE NEPHRON
- THE ON-GOING PROCESS OF NEPHON FAILURE LEADS TO CHRONIC RENAL FAILURE
24
Q
Psoriasis
A
- DISORDER OF THE SKIN CHARACTERIZED BY RAISED AREAS OF ABNORMAL TISSUE THAT IS AUTOIMMUNE IN NATURE.
- TYPICALLY THE SKIN IS RED TO PURPLE, DRY, RAISED, AND ITCHY
25
Types of Psoriasis
* PLAQUE
* GUTTATE
* INVERSE
* PUSTULAR
* ERYTHRODERMIC
26
Plaque Psoriasis
* TYPICALLY 90% OF CASES
* PRESENTS AS RED PATCHES WITH WHITE SCALES ON TOP
27
Guttate Psoriasis
* NUMEROUS SMALL SCALY RED OR PINK PAPULES
* DROP-SHAPED LESIONS
* SPREAD OVER LARGE AREAS OF THE BODY:
* PRIMARILY THE TRUNK, LIMBS AND SCALP
* LESIONS ARE OFTEN TRIGGERED BY STREPTOCOCCAL NFECTONS
28
Pustular Psoriasis
* PRESENTS AS SMALL NON-INFECTIOUS, PUS-FILLED BLISTERS
* SKIN UNDER THE PUSTULES IS USUALLY RED AND TENDER
* PUSTULES MAY BE LOCALIZED OR WIDESPREAD
29
Inverse Psoriasis
* FORMS RED PATCHES IN SKIN FOLDS
* PATCHES ARE SMOOTH AND INFLAMED
30
Erthrodermic Psoriasis
* WIDESPREAD FORM OF THE DISORDER THAT MAY ARISE FROM ANY OF THE OTHER TYPES. – OFTEN 90% OF BODY SURFACE
* WIDESPREAD EXFOLIATIONOF THE SKIN
* OFTEN WITH SEVERE DRYNESS, ITCHING, SWELLING AND PAIN
* MAY BE FATAL AS THE EXTREME INFLAMMATION AND EXFOLIATION DISRUPTS THE BODY’S ABILITY TO REGULATE TEMPERATURE AND PERFORM BARRIER FUNCTION
31
Sebhorrhic-Like psoriasis
* FORM WITH CLINICAL ASPECTS OF PSORIASIS AND SEBORRHEIC DERMATITIS
* FORMS RED PLAQUES
* GREASY SCALES ESPECIALLY IN AREAS SUCH AS SCALP, FOREHEAD, SKIN FOLDS NEXT TO THE NOSE, SKIN AROUND THE MOUTH, ABOVE THE STERNUM AND IN GENERAL SKIN FOLDS
32
Psoriasis in Nails
* PITTING OF NAILS
* WHITENING OF THE NAISL
* SMALL AREAS OF BLEEDING FROM CAPILLARIES UNDER THE NAILS
* YELLOW-REDDISH DISCOLORATION OF NAILS
* THICKENING OF SKIN UNDR THE NAILS
* LOOSENING AND SEPARATION OF NAIL
* CRUMBLING OF THE NAIL
33
Psoriatic Arthritis
* A FORM OF CHRONIC INFLAMMATORY ARTHRITIS
* ASSOCIATED WITH PSORIASIS OF THE SKIN AND NAILS
* INVOVLES PAINFUL INFLAMMATION OF THE JOINTS AND SURROUNDING CONNECTIVE TISSUE
* CAN OCCUR IN ANY JOINT – MOST COMMON IN FINGERS AND TOES
* MAY ALSO AFFECT HIPS, KNEES, SPINE AND SACROILIAC JOINTS
34
# Psoriasis
Causes
* NOT CLEARLY UNDERSTOOD
* AUTOIMMUNITY
* GENETICS
* INDIVIDUALS OFTEN HAVE FAMILY HISTORY
35
Patho of Psoriasis
* STARTS WITH THE INITIATION PHASE – MAY BE SKIN TRAUMA, INFECTION OR IN SOME CASES, DRUGS
* INITIATION PHASE SEEMS TO LEAD TO ACTIVATION OF THE IMMUNE SYSTEM
* SKIN CELLS ARE REPACED IN 3-5 DAYS (NORMAL IS 28-30) – PROBABLY CAUSED BY PREMATURE MATURATION OF KERATINOCYTES
* THE MATURATION RATE IS ALTERED BY INITIATION OF INFLAMMATORY CASCADE IN THE DERMIS
* DNA RELEASED FROM DYING CELLS MAY ACT AS AN INFLAMMATORY STIMULUS
* DENDRITIC CELLS ARE INCREASED IN PSORIASIS
36
# Psoriasis
Patho Appearance
* SKIN IS THICKENED WITH HYPERKERATOSIS AND PARAKERATOSIS
(PERSISTENCE OF NUCLEI IN CELLS OF THE STRATUM CORNEUM)
* NUCLEATED LAYERS OF THE THE EPIDERMIS ARE THICKENED
SEVERALFOLD
* IN CHRONIC LESIONS DERMAL PAPILLAE MAY APPEAR AS BULBS
INSTEADE AS CONES
* CAPILLARIES OF THE DERMAL PAPILLAE ARE DILATED AND TORTUOUS
37
Acne vulgaris
CHRONIC SKIN DISORDER OF HAIR FOLLICLES THAT OCCURS
DUE TO BLOCKAGE BY SKIN CELLS AND SEBUM
38
Comedome
- clogged hair follicle
- provides environment for growth of commensal skin bacteria
- start as microcomedomes
- enlarged microcomedomes = pimples
39
Pimples
* WHITE HEADS: DEEP MICROCOMEDONE
* BLACKHEADS: SUPERFICIAL MICROCOMEDONE, OPEN TO AIR, WITH OXIDATION OF MELANIN
40
# Acne
Risk Factors
- mainly inherited
- genetic control of androgen production
- sebum production
41
# Acne
Role of Hormones
BOTH ANDROGENS AND IGF-1 MAY BE ESSENTIAL FOR THE
DEVELOPMENT OF ACNE, AS ACNE DOES NOT DEVELOP IN
INDIVIDUALS WHO LACK ANDROGEN SENSITIVITY
42
# Acne
Role of bacteria and mites
- SPECIFIC SUBSTRAINS OF C. ACNES THAT ARE ASSOCIATED WITH NORMAL SKIN AND OTHER SUBSTRAINS THAT ARE ASSOCIATED WITH ACNE
- INFECTIONS WITH THE MITE DEMODEX, IS ALSO ASSOCIATED WITH THE FORMATION OF ACNE
43
# Acne
Causes of Blocked Hair follicles
* INCREASED SEBUM PRODUCTION
* EXCESSIVE DEPOSITION OF KERATIN PROTEIN
* FORMATION OF A COMEDO
* COLONIZATION OF THE FOLLICLE BY BACTERIA – USUALLY CUTIBACTERIUM ACNES
