Reading...
Play button
Play button
Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
191 Cards in this Set
- Front
- Back
|
Definition inflammation?
|
Protective reaction of vascular tissues to a exogenous or endogenous injuorous stimuli
|
|
|
Purpose of inflammation?
|
1. Eliminate
2. Dilute 3. Wall off The injurours agent |
|
|
Inflammation or uterus?
|
Metritis
|
|
|
Inflammation of vagina?
|
Kolpitis
|
|
|
Inflammation of kidneys?
|
Nephritis
|
|
|
Inflammation of tounge?
|
Glossitis
|
|
|
Inflammation of lips?
|
Cheilitis
|
|
|
2 localizations of inflammation and main cause?
|
Local - mild injury
Systemic - severe injury |
|
|
What ways may we classify inflammation?
|
According to:
1. Time spectrum 2. Inflammation pattern 3. Histological features 4. Causative agent |
|
|
Classification according to time spectrum?
|
1. Hyperacute
2. Acute 3. Subacute 4. Subchronic 5. Chronic |
|
|
Classification according to the 3 steps of inflammation?
|
1. Alterative inflammation
2. Exudative inflammatino 3. Proliferative inflammation |
|
|
What is alterative inflammation?
|
Inflammation in necrosis - due to tissue injury
|
|
|
Examples of alterative inflammation?
|
Viral hepatitis
Diptheria (URT, caused by Corynebacterium diphtheriae) |
|
|
What is exudative inflammation?
|
Formation of inflammatory fluid: exudate
Protein rich, since capillary permeability increase |
|
|
3 types of exudate?
|
Water - serous
Fibrin - fibrinous Pus - suppurative |
|
|
Examples of exudative inflammations?
|
- Simple cold
- Bronchitis - Expectoratinos - Diarrhea |
|
|
What is proliferative inflammation?
|
Formation of granulation tissue & scar (fibrosis)
|
|
|
Examples of proliferative inflammation?
|
Chronic cholecystitis - leading to thickened wall - associated with stones
|
|
|
Inflammation according to histological features / specificity?
|
1. Non-specific - most of them
2. Specific - very few |
|
|
What is a non-specific inflammation?
|
An inflammation where we are not histologically able to detect the causative agent
|
|
|
Another name for specific inflammation?
|
Granulomatous inflammation
|
|
|
Examples of specific / granulomatous inflammation?
|
TBC - with presence of Langhans cells
|
|
|
What are macrophages, histiocytes and langhans cells?
And what about epithelioid cells? |
Macrophages:
- Phagocytic cells derived from monocytes, which acts like APC for T-cells - initiating immune reaction Histiocytes - Macrophages that have entered tissue (histo = tissue). These cells are the ones in a granuloma - and are often referred to as epitheloid cells Langhans cells - These are simply fused histiocytes - forming multinucleated giant cells |
|
|
How does a epithelioid histiocyte differ from a normal macrophage?
|
Slightly larger, larger nucleus, more eosinophilic. Changes are thought to be caused by already changed into APC
|
|
|
Classification according to causative agent?
|
1. Septic
2. Aseptic |
|
|
Septic inflammation - cause and purpose?
|
Cause is always any microbe
Purpose is to protect |
|
|
Aseptic inflammation - cause and purpose?
|
Cause is a wide variety of things, but typically chemical substances.
Has a reparative function - so thickening (congelation) occurs due to granulation tissue |
|
|
Clinical presentation of acute inflammation?
|
Local signs
- Calor, rubor Systemic - Fever, leucocytosis Ab - White body reaction Involvement of lymphatic tissue - Cervical lymphadenopathy = angina |
|
|
Definition leucocytosis?
|
9000-30 000 cells pr mm^3
And due to rapid formation, some of them may be immature (band form) - they are not segmented This is a left shift feature! |
|
|
5 cardinal signs of inflammation - according to Celsus in 1st century BC?
|
1. Calor
2. Rubor 3. Dolor 4. Tumor 5. Functio laesa |
|
|
What are the general signs always present in inflammation?
|
1. Fever
2. Leukocytosis 3. CRP |
|
|
How does inflammation cause fever?
|
Irritation of thermoregulation center
Raise the set-point for thermoregulatory system: 1. Shivering & peripheral vasoconstriction since set-point is higher than real temperature 2. Sweating and vasodilation when set-point is back to normal - and irritation is stopped |
|
|
What is leukocytosis?
|
Increased WBC count
|
|
|
Which leukocytes increase in:
Bacteria? Parasites? Virus? |
Bacteria - neutrophils
Parasites - eosinophils Virus - lymphocytes |
|
|
What may cause leukopenia?
|
- Viral infections
- Salmonella infections - Rickettsioses |
|
|
Which substances may irritate thermoregulatory center and cause fever?
|
TNF
IL-1, IL-6 |
|
|
What is normal neutrophil count?
|
4-9 x 10^9 /L
|
|
|
WHat is a leukemoid reaction - in normal boundaries?
|
30-40 x 10^9 /L
|
|
|
What are the 3 main changes in acute inflammation?
|
1. Vascular changes
2. Increased vessel permeability 3. Endothelial injury |
|
|
What are the vascular changes in acute inflammations?
|
1. Arteriolar vasodilation (rubor, calor)
2. Increased permeability of vessels 3. Leukocytic injury of endothelial vessels |
|
|
How does inflammation cause increased permeability of vessels?
What does it lead to? |
1. Wider intercellular junctions
2. Retraction of endothelial cells (Histamin, bradykinin...) Lead to: 1. Transudate (edema - protein poor) 2. Exudate (protein rich) |
|
|
What is the consequence of leukocyte dependent endothelial injury?
|
1. Proteolysis --> Protein leakage --> Platelet adhesion & thrombosis
|
|
|
Definition infiltrate?
|
Cellular components from capillary fluid have migrated to intestitium
|
|
|
What are the cellular events in acute inflammation?
= How the neutrophils migrate to area of inflammation |
1. Leukocyte marginatino
2. Transmigration 3. Chemotaxic 4. Phagocytosis 5. Passive migration of RBC |
|
|
What is leukocyte margination?
|
Neutrophils roll along vessel wall - goes quite quick - 1 day.
Later the mono/macrophages come. |
|
|
What is transmigration?
Why does the neutrophils migrate first? |
The diapedesis (in venules)
Neutrophils migrate first since they contain granules with lytic enzymes - which engulf microbe and fuse it with the lysosomes. |
|
|
What are the endogenous chemotactic agents?
|
IL's, complement 5a
|
|
|
What are the exogenous chemotactic agents?
|
Toxins, bacterial proteins
|
|
|
What is an abscess with pus?
|
What is created when neutrophils have migrated - and cause lysis of microbe.
The pus accumulation consist of: - Dead cells - Neutrophils - Microbes And the area is sometimes walled off - by necrotic circle and thus fibrosis by granulation tissue |
|
|
What are RBC's function in inflammation?
|
They cannot move - and have no role - other than in hemorrhagic inflammation - when they escape through capillary walls
|
|
|
3 phases of phagocytosis?
|
1. Recognition & attachment
2. Engulfment 3. Killing and degradation |
|
|
How is recognition and attachment done?
|
Via opsonins: IgG, C3b
|
|
|
How is engulfment one?
|
Pseudopods formed => Phagocytic vaguole + lysosome = Phagolysosome
|
|
|
How is killing of microbe done?
|
Oxidative burst: Reactive oxygen metabolites
- Superoxide - Hydrogen peroxide - Hypochlorous radicals Lysozymes In some highly virulent microbes both lekocyte and micro die! |
|
|
Example of highly resistant microbes?
|
TBC - they persist within macrophage and are reactivated after many years
|
|
|
What is responsible for rolling of neutrophils?
|
Selectins
|
|
|
What is responsible for attachment of neutrophils?
|
Integrins
|
|
|
What are the 4 possible outcomes of acute inflammation?
|
1. Resolution
2. Healing by scar 3. Abscess formation 4. Progress into chronic inflammation 5. Death |
|
|
What is resolution?
Examples? |
Restoration to normal
- Neutralize chemical substances - Apoptosis of inflammatory cells |
|
|
When is inflammation healed by scar / granulation tissue?
- Fibrinous inflammation? - Purulent inflammation? |
When tissue is destroyed
Fibrinous -Adhesions - Fibrosis Purulent - Abscess formation |
|
|
What does an abscess consist of?
|
Pus, pyogenic membrane
|
|
|
What is pus?
|
Yellowish liquid consisting of dead white cells, dead microbes, necrotic debris… fibrinous debris
|
|
|
What is a pyogenic membrane?
|
The inner lining of an abscess with not yet autolyzed cells.
|
|
|
In what cases may an acute inflammation proceed to chronic one?
Examples? |
In repeated attacks:
1. Bronchitis --> Chronic bronchitis 2. Otitis --> Chronic otitis 3. Hepatitis --> Chronic hepatitis 4. Nephritis --> Chronic nephritis 5. Abscess --> Chronic abscess |
|
|
Which cases may acute inflammation lead to death?
|
1. Acute myocarditis
2. Acute encephalitis |
|
|
What are the causes of an inflammation becoming chronic?
|
1. Persistent organism in body
2. Repeated attack of acute inflammation 3. Autoimmune reactions 4. Exposure to inorganic material |
|
|
Examples of persistent bacteria in body?
|
M. TBC --> Tuberculosis
|
|
|
Examples of foreign body chronic inflammation?
|
- Inhalation of silica --> Silicosis
- Suture remnants --> Schlemm's tumor - Woods, metals etc... |
|
|
Examples of autoimmune reactions - where immune system have previously formed Ab against microbes - cross react to attack its own tissues?
|
1. Rheumatoid arthritis
2. Gastric mucosa --> Gastritis 3. Glomeruli --> Glomerulonephritis 4. Multiple sclerosis |
|
|
What are the typical cells in chronic inflammation?
|
Round cell infiltrate:
- Lymphocytes - Macrophages - Plasma cells (from B-ly --> Secrete Ig) |
|
|
Name some monocyte-macrophage cells?
|
Siderophages (iron consumpted)
Gitter cells (brain) Mucophages |
|
|
Some long term effects of chronic inflammation?
|
1. Scarring fibrotic tissue
2. Granulomatous (specific) inflammation (later) |
|
|
What is erythema?
|
Redness of skin / mucous membrane due to hyperemia of underlying capillaries
|
|
|
What is serous inflammation?
|
Effusion of watery serous fluid from blood plasma or produced by mesothelial cells of serous membranes
|
|
|
What is granulomatous inflammation?
|
Usually chronic and specific inflammation - with granuloma formation
|
|
|
What is catarrhal inflammation?
|
Inflammation of the mucus membranes of airways or cavities, by hyperemia, edema, exudation and gland proliferation
|
|
|
What is fibrinous inflammation?
|
Inflammation with increased vascular permeability - so fibrin leaks out and fibrinous exudate is deposited
May convert to a scar, usually |
|
|
What is suppurative inflammation?
|
Inflammation with marked pus formation
|
|
|
What is purulent inflammation?
|
Inflammation with large amounts of pus (neurtophils, dead cells, fluid) - and if it is closed = Abscess
|
|
|
What is pseudomembranous inflammation?
|
Inflammation in response to a necrotizing toxin (like diphteria) - which create a detached false membrane composed of:
- Fibrin - Necrotic tissue - Dead WBC |
|
|
What is ulcerative inflammation?
|
Inflammation close to epithelium - lead to necrotic loss of surface layers
|
|
|
What is gangernous inflammation?
|
Inflammation caused by a putrefactive bacteria - causing cell death
|
|
|
What is proliferative inflammation?
|
Inflammation leading to new production of tissue (mostly scar formation)
|
|
|
What is always found on top of ulcers?
|
Fibrin layer
|
|
|
Example of fibrinous inflammation?
|
Fibrinous pericarditis of heart - looking like bread & butter
|
|
|
Examples of catarrhal inflammation?
|
Bronchitis
Rhinitis (normal flu) |
|
|
Example of serous inflammation?
|
Pleuritis
|
|
|
What are macrophages in lung called?
|
Koniophages - eating dust
|
|
|
What are macrophages eating iron called?
|
Siderophages
|
|
|
What are macrophages eating fat droplets called?
|
Lipophages (foamy cells)
|
|
|
What are macrophages eating mucus called?
|
Mucophages
|
|
|
How do you classify the morphological patterns of inflammation?
|
1. Alterative
2. Exudative 3. Proliferative |
|
|
Type of alterative proliferations?
|
1. Acute anterior poliomyelitis
2. Diphterial myocarditis (!) |
|
|
5 types of exudative inflammations?
|
1. Serous
2. Fibrinous 3. Suppurative 4. Necrotizing / gangrenous 5. Non-purulent |
|
|
Classification of proliferative pattern of inflammation?
|
1. Primary (rare)
2. Secondary (cholecystitis) |
|
|
Definition serous inflammation?
|
Effusion of watery fluid from blood plasma or produced by mesothelial cells of serous membranes
Low in protein |
|
|
Examples of serous inflammation?
|
- Skin blisters
- Rhinitis - Serous membranes: o Pericarditis o Pleuritis |
|
|
What is a fibrinous inflammation?
|
Inflammation where, due to greater permeability of capillaries, larger proteins like fibrinogen leaks out and is deposited as fibrin
This forms pseudomembranes |
|
|
What does pseudomembranes consist of?
|
Fibrin
Necrotic mucosa Etiologic agents Leukocytes |
|
|
Examples of fibrinous inflammation (with pseudomembrane)?
|
- Diphteria, dysentery
- Pericarditis - Lobar pneumonia |
|
|
Etiological agents of diphteria?
|
Corynebacterium
|
|
|
Etiological agent of dysentery?
|
Shigella species
|
|
|
How do you call a heart with fibrinous inflammation?
|
- Cor villosum
- Cor hirutum Both the same |
|
|
Etiological agent of lobar pneumonia?
|
Streptococcus pneumoniae
|
|
|
What does healing of fibrinous inflammation depend on?
|
Thickness of fibrin layer
|
|
|
In thin fibrinous inflammation - how is it healed?
|
Fibrinolysis & fluid removal by capillaries
|
|
|
In thick fibrinous inflammation - how is it healed?
|
Organization with granulation tissue and scarring
|
|
|
What is granulation tissue?
|
Forming of new CT and blood vessels by migration of fibroblasts and endothelial cells
|
|
|
What are the possible complications of fibrinous inflammation of serous membranes?
|
1. Adhesions
2. Occlusions |
|
|
When does fibrinous inflammation cause adhesions?
|
If thickening remains at e.g. pericardium
=> Fibrinous adhesions |
|
|
When does fibrinous inflammation cause occlusion of serous cavity?
|
If fibrin is not removed - cause adhesions and occlusion.
In heart it leads to restrictive pericarditis - also called cor petrosum I think... |
|
|
What is a mix between serous and fibrinous inflammation called?
|
Serofibrinous - when exudate is composed of both.
|
|
|
What is a suppurative inflammation?
|
Inflammation with a lot of pus as exudate - so leads to suppuration
|
|
|
What is pus?
|
Fluid with dead bacteria, dead liquefied cells, neutrophils
|
|
|
Which bacteria are so-called pyogenic?
|
- Staphylococci (most important)
- Streptococci - Pneumococci - Gonococci - Gram negative bacilli |
|
|
Classification of suppurative inflammation?
|
1. Superficial
2. Deep |
|
|
Examples of superficial suppurative inflammation?
|
- Skin = Folliculitis
- Mucus - Serosa = Meningitis, pericarditis - Membranes - Meninges |
|
|
Examples of suppurative inflammation of mucosa?
|
- Bronchitis
- Sinutisis - Enterocolitis - Salpingitis / kolpitis / metritis |
|
|
2 classifications of deep suppurative inflammation?
|
1. Abscess
2. Phlegmone |
|
|
Definition abscess?
What is causative agent? |
Pus-filled cavity caused by suppurative inflammation, lined by a fibrinous membrane
Causative agent is staphylococci |
|
|
If an abscess is not drained - what happens?
|
It becomes a chronic abscess - lined by a fibrous capsule (pyogenic membrane)
|
|
|
What is a phlegmone?
|
A diffuse / not circumscribed inflammation of interstitial tissue - also called cellulitis
|
|
|
What is empyema?
|
Accumulation of pus in a already formed body cavity - like thoracic cavity or gall bladder or pleural cavity
|
|
|
How may a superficial suppurative inflammation become deep?
|
1. Hematogenous
2. Lymphogenous 3. Trauma |
|
|
How is the fluid in phlegmone inflammation?
|
Brownish watery exudate - but not pus
|
|
|
What is the etiological agent of phlegmone?
|
Beta hemolytic streptococci
|
|
|
What is a fistula?
|
A pathological connection between 2 body cavities. Can be created by a spontaneous rupture of an abscess.
|
|
|
3 complications of suppurative inflammation?
|
1. Bacteremia
2. Septicemia 3. Pyemia / embolization 4. Thrombophlebitis 5. Lymphangitis |
|
|
What is bacteremia?
|
Presence of bacteria in blood - but with no immediate clinical symptoms since they are removed by monocyte/macrophage system
|
|
|
What may be the causes and complications of bacteremia?
|
Causes
- Tooth brushing - Heavy meals Complications - Become valve vegetations --> Infective endocarditis - Meningitis - Brain abscesses |
|
|
What is sepsis / septicemia?
|
Massive bacteremia - presents with clinical symptoms of fever & leukocytosis
May be the cause of death |
|
|
What is pyemia?
|
Presence of pus in blood - basically metastatic abscesses!
(thrombi with bacteria) |
|
|
Classification of pyemia?
|
1. Central
2. Peripheral |
|
|
What is central pyemia?
|
Metastatic abscess from endocarditis - occludes somewhere else and cause a new abscess formation
|
|
|
What is peripheral pyemia?
|
Metastatic abscess with source from peripheral veins (often varicose) - cause thrombosis and abscess of lungs
|
|
|
Name empyema of pleura?
|
Suppurative pleuritis
|
|
|
Name empyema of appendix?
|
Suppurative appendicitis
|
|
|
Name empyema of gall duct?
|
Suppurative cholecystitis
|
|
|
What is thrombophlebitis?
|
An abscess has reached a vein and it cause a secondary inflammation - with subsequent thrombosis.
|
|
|
What is a pseudomembranous inflammation?
|
Inflammation in response to some necrotizing bacteria - creating a detached false membrane, consisting of fibrin, necrotic tissue and dead WBCs
|
|
|
What bacteria may cause pseudomembranous inflammation? (classification)
|
1. Corynebacterium diphteriae (pharynx)
2. Shigella dysenteriae (GIT) 3. Candida (immunocompromized, oral cavity) |
|
|
What happens to the pseudomembrane?
|
1. Tear off and detach
2. Become ulcerated 3. Heal by granulation tissue and fibrosis |
|
|
What is the agent, location and consequence of diphteria caused pseudomembranous inflammation?
|
- Larynx / pharynx
- Corynebacterium diphteriae - May cause suffocation due to swelling or myocarditis due to toxins selecting cardiac muscle |
|
|
What is agent, locatino and consequence of dysentery caused pseudomembranous inflammation?
|
- GIT
- Enterocolitis - Danger of rupture and peritonitis - Shigella dysenteriae |
|
|
How is a candida pseudomembranous inflammation - and where?
|
Presents with white/yellow pseudomembrane on
- Tounge (glossitis) - Esophagus (esophagitis) in immunocompromized patients! |
|
|
What is a gangrenous inflammation?
|
A secondary change by putrefactive bacteria - which cause cell death of the surface of mucosa
Also here risk of perforation - due to necrotic cell wall that is not flexible |
|
|
Which typeso f gangrene do we speak of?
|
Wet gangrene
|
|
|
Appearance of tissues in wet gangrenous inflammations?
|
Yellow, soft and liquid
|
|
|
Examples of typical wet gangrenous inflammations?
|
- Appendicitis
- Cholecystitis |
|
|
Definition granulomatous inflammation?
|
A inflammation characterized by granulomas
|
|
|
Ok.. So what is a granuloma?
|
A granuloma is a collection of histiocytes and macrophages - which are activated and trying to eat something it cannot
|
|
|
What type of immune reaction is granulomatous inflammation?
|
Obviously - a cell mediated and delayed.
|
|
|
What are these macrophages called?
|
They are called epithelioid cells - and when they fuse together they are called Langhans multinucleated giant cells
|
|
|
So how does a granuloma look?
How does it reflect the function? |
Center Langhans cells
Around epithelioid cells Circle of lymphocytes around So it shows that it does not eliminate agent - but wall it off |
|
|
What 5 main things are causing granulomatous inflammation? (classification)
|
1. Bacteria
2. Parasites + funghi 3. Inorganic meteals or dust 4. Foreign body 5. Unknown substance |
|
|
Examlpe of 3 bacterias causing gr.inflamm?
|
- TBC
- Leprosy - Syphilis (3rd stage) |
|
|
Another name for M.TB and what are the 3 types?
Which can humans be infected by? |
Koch bacillus
1. Bovine (cows) 2. Avian (birds) 3. Human Human can be infected by all! |
|
|
How are humans infected by TBC?
|
1. Inhalation
2. Drinking infected mils 3. .Eating (rare) 4. Autoinfection - you expectorate and swallow |
|
|
How does a TB granuloma look?
|
Central casseous necrosis of the granuloma
|
|
|
Definition tuberculosis?
|
An infectious disease characterized by growth of nodules (tubercles) in tissue - particularly the lungs
|
|
|
How does tb nodules look grossly?
|
Grey, 1-2 mm with central casseous necrosis and calficications
|
|
|
How does TB nodule look in LM?
|
1. Central caseous necrosis
2. Macrophages (epithelioid cells) --> Langhans cells 3. Lymphocytic rim |
|
|
How is the TBC exudate?
|
Serofibrinous exudate
|
|
|
2 classifications of TBC according to time?
|
1. Primary - proliferate in macroph. - scarring & calcification
2. Secondary - reactivated calcified nodule - often in immunocompromized state 3. Miliary - tuberculous septicemia |
|
|
Definition leprosy?
|
A contagious infectious disease affecting skin, mucous membranes and nerves, causing discoloration and lumps.
Sometimes even cause deformities. |
|
|
Leprosy is caused by which agent?
|
Mycobacterium leprae
|
|
|
Classification of leprosy?
|
1. Lepromatous leprosy
2. Tuberculoid leprosy |
|
|
What is lepromatous leprosy?
|
Contagious form - with skin lesions.
M.Leprea reside in macrophages (called Virchow cells) and in viscera |
|
|
What is tuberculoid leprosy?
|
Sterile form - m. leprae reside in schwann cells of peripheral nerves
Cause tuberculoid granulomas |
|
|
What is the cause of death in leprosy?
|
Secondary infections + amyloidosis
|
|
|
Definition syphilis?
|
Chronic contageous bacterial disease
|
|
|
Agent in syphlis?
|
Treponema pallidum
|
|
|
Ways of infection by syphilis?
|
1. STD
2. Transplacental fetus infection |
|
|
How does the artery lesions of syphilis look in LM?
= Proliferative endarteritis |
Proliferative endarteritis:
- Endothelial hypertrophy - Fibrosis of t. intima - Local ischemia - Inflammation (plasma cells) |
|
|
Gumma lesion is typical growth for grade 3 syphilis. It looks like a really bad wound, like on nose
How does it look in LM? |
1. Central coagulative necrosis
2. Specific granulation tissue 3. Fibrous tissue |
|
|
How is manifestation of primary syphilis?
|
Chancre = Contagious ulcus durum (hard ulcers) on penis (m) or vagina/cervix (f)
They are painless, firm ulcerations with regional painless lymphadenopathy. Will spontaneously resolve after a few weeks - and leave a scar. |
|
|
Manifestation of secondary syphilis?
Time Lymph nodes. Lesions Condylomata lata |
After about 2 months - also contagious period
Generalized lymphadenopathy + various mucocutaneous lesions Condyloma lata (wart-like lesions in genital area): - Anogenital region - Inner thighs - Oral cavity |
|
|
Time of manifestation of tertiary syphilis?
|
5 years!
|
|
|
3 main manifestations of tertiary syphilis?
|
1. Cardiovascular - syphilitis aortitis
2. Neurosyphilis - tabes dorsalis + general parastesia 3. Gumma - ulcerative lesions |
|
|
What is syphilitic aortitis?
|
Endarteritis of vasa vasorum (of proximal aorta!)
Lead to scarring of media (due to ischemia) --> Dilation -----> Aneurysm (of thoracic!) |
|
|
What is tabes dorsalis & general parastesia - the so-called 'neurosyphilis'?
|
1. Degeneration of posterior columns of spinal cord (they look black myslim)
--> Lead to sensory and gait abnormalities 2. Cortical atrophy --> Lead to psychic troubles |
|
|
Where do you get gummas in 3rd stage of syphilis?
|
- Bone
- Skin - Mucosa (oral cavity) |
|
|
3 fates of congenital syphilis?
|
1. Abortus
2. Early syphilis (infantile) 3. Late syphilis |
|
|
How is fetus aborted in congenital syphilis?
|
1. Hepatomegaly
2. Pancreatitis 3. Pneumonia alba (inflamm & fibrosis of lungs) |
|
|
Signs of early congenital syphilis?
|
1. Chronic rhinitis
2. Mucocutaneous lesions |
|
|
Signs of late congenital syphilis?
|
Hutchinson triad:
1. Filed down central incisors 2. Keratitis (blindness) 3. Deafness (CN VIII injury) |
|
|
Characteristics of Cat-scratch disease granulomas?
What is agent? |
1. Cat scratch
2. Lymph nodes draining the scartch are granulomatous 3. Form pus (suppurations) Agent is bartonella henslae |
|
|
How are sarcoidosis granulomas?
|
Similar to TB ones - but non-caseating - and instead surrounded by fibrous tissue ring
|
|
|
Another name for Wegener's granulomatosis? Which we now shall use - since Wegener is out !
|
GPA = Granulomatosis with Polyangitis
|
|
|
RIsk factors for chronic cholecystitis?
4F's |
Female
Fat Forty Fertile |
|
|
When you have transverse ulcers in small bowel - what does it '100%' mean?
|
TB!
From swallowing of expectorated TB . |
