First Aid Immunology/ Psychiatry Flashcards
3 main features of Wiskott-Aldrich Syndrome
X-linked recessive
WATER: Wiskott-Aldrich
Thrombocytopenia (20-50k) => easy bruising, petechiae, purpura, epistaxis
Eczema
Recurrent infection
Effect of C1 esterase deficiency
Hereditary angioedema b/c allows activation of something that causes huge bradykinin release
-ACEi are contraindicated in these pts
Name two negative acute phase reactants (downregulated by inflammation)
Serum proteins whose concentrations decrease in response to inflammation
- albumin: decrease production to conserve amino acids for the positive reactants (ex: CRP, ferritin, hepcidin, fibrinogen)
- transferrin: internalized by macrophages to sequester iron intracellularly
Which antibodies are involved in each of the 4 types of hypersensitivity reactions
ACID
Type I: Atopy and anaphylaxis (IgE)
Type II: Cytotoxic (IgG and IgM)
Type III: Immune complex (IgG)
Type IV: delayed
Type IV is the only one that doesn’t use antibodies (cell mediated)
Which exposures have preformed antibodies that can be given to unvaccinated patients?
“To Be Healed Very Rapidly”
- tetanus
- botulinum
- HBV
- Varicella
- Rabies
Given passive immunity
Name two inhibitors/checks on the complement pathway
- Cd55 = DAF = decay-accelerating factor
- C1 esterase inhibitor
Both work to inhibit complement activation to reduce: response to self-cells and spontaneous activation
Give a clinical use of the following recombinant cytokines
(a) IFN-alpha
(b) IFN-beta
(c) IFN-gamma
(d) erythropoietin
(a) IFN-alpha used in chronic Hep B/C, Kaposi sarcoma
(b) IFN-beta in multiple sclerosis
(c) IFN-gamma in chronic granulomatous disease
(d) Erythropoietin in anemia (esp in renal failure)
Differentiate what innate and adaptive immunity use for pathogen recognition
Innate immunity uses toll-like receptors that recognize patterns associated w/ pathogens
Adaptive immunity use memory cells whereby first exposure produces a stronger and quicker immune response the next time
3 yo w/ recurrent severe ear infxn
- multiple telangiectasias on face
- walks w/ difficulty, truncal instability
Dx
Dx = ataxia-telangectasia = primary immunodeficiency of both B and T cells 2/2 mutation in ATM gene (DNA repair enzyme)
A’s:
- Ataxia (2/2 cerebellar atrophy)
- IgA deficiency => recurrent sinopulmonary infxn
- Spider Angiomata
- ATM gene mutation
Chronic granulomatous disease
(a) Pathophysiology
(b) Increased risk of what infections
Chronic granulomatous disease
(a) Variety of congenital diseases w/ defective phagocytic NADPH (used to make ROS) => inability to kill certain ingested pathogens
(b) Increased risk of catalase positive species (ex: S. aureus, pseudomonas) and fungi (Aspergillus)
7 yo pt s/p MVA receives blood transfusion to which she develops SOB and oral-facial swelling
- wheezing on exam and atopic dermatitis
- Hx: recurrent ear and lung infection
Dx
Dx = Selective IgA deficiency
- anaphylaxis in response to products containing IgA
- recurrent infection (specifically upper respiratory)
Risk of live attenuated vaccine
Reversion to virulent form
What type of hypersensitivity rxn is
(a) Hyperacute transplant rejection
(b) Graft-vs-host disease
(a) Hyperacute transplant rejection (within minutes) is a type I hypersensitivity rxn 2/2 preformed antibodies
(b) Graft-vs-host is a delayed cellular response = type IV hypersensitivity
Where do the following mature
(a) T cells
(b) B cells
(a) T cells mature in the thymus
(b) B cells mature in the bone marrow
Define acute phase reactant
(a) Induced by what?
(b) Location of production
Acute phase reactant is a serum protein whose concentration changes significantly in response to inflammation
(a) Induced by IL-6
(b) All produced by the liver
Which of the following type of hypersensitivity reaction is responsible for the following
(a) Graves disease
(b) Arthus rxn to tetanus vaccine
(c) Pernicious anemia
(d) SLE
(e) Poison ivy
(f) Graft vs. host
(g) Goodpasture syndrome
Hypersensitivities
(a) Graves- type II (direct cytotoxic)
(b) Arthus rxn to tetanus vaccine is type III (immune complex mediated)
(c) Pernicious anemia- type II
(d) SLE type III
(e) Poison ivy = contact dermatitis = type IV (cellular, delayed)
- not atopic!! be careful
(f) Graft vs. host- type IV (delayed, cellular)
(g) Goodpastures- cytotoxic type II
Describe how DAF deficiency causes paroxysmal nocturnal hemoglobinuria
CD55 (DAF = decay-acclerating factor) is a factor that works to inhibit complement activation to self cells, w/ CD55 deficiency you get complement-mediated breakdown of RBCs => paroxysmal nocturnal hemoglobinuria
Main fxn of interferon alpha and beta
(a) Secreted by what?
Interferon alpha and beta are secreted by virally infected cells to act locally on uninfected cells
Basically work against viral infections
-cause apoptosis locally to disrupt viral amplification
Name the d/o associated w/ the following autoantibodies
(a) Anti-basement membrane
(b) Antiparietal cell
(c) Antimitochondrial
(d) Anti-smooth muscle
(e) Anti-SSA/SSB
Autoantibodies
(a) Anti-basement membrane = Goodpastures
(b) Antiparietal = Pernicious anemia
(c) Primary biliary cirrhosis (PBC)
(d) Antimitochondrial = autoimmune hepatitis
(e) Anti-SSA/SSB = Sjogrens
3 mo old referred for recurrent sinopulmonary infection, flow cytometry shows decrease in CD40L
(a) Dx
(b) Antibody profile expected
(a) HyperIgM Syndrome
- lack of CD40L causes inability to class switch
- p/w severe pyogenic infections early in life
(b) High IgM w/ very low IgG, IgA, and IgE
What two molecules are the primary opsonins of the complement system
Primary opsonins = C3b (binds bacteria directly) and IgG
-work to enhance phagocytosis
Fungal/parasitic infxn seen in dif immunodeficiencies
(a) T cell d/o
(b) B cell d/o
(c) Granulocyte d/o
(a) See local candida and PCP w/ reduced T cells
(b) GI giardiasis w/ B cell d/o (ex: recurrent GI infxn in selective IgA deficiency)
(c) Granulocyte d/o => systemic candida, aspergillus
X-linked agammaglobulinemia
a) Differentiate from selective IgA deficiency
(b) Differentiate from common variable immunodeficiency (CVID
B cell disorders
(a) X-linked agammaglobulinemia will show reduced serum levels of all Ig classes, while selective IgA deficiency will have low IgA but normal IgE and IgG
(b) X-linked agammaglobulinemia presents earlier (like at 6 mo) while CVID often presents later, CVID has normal number of B cells
- both are defects in B cell maturation
What is anergy?
(a) Importance
Anergy = state of inactivity, immune cell cannot be activated by its antigen
-occurs when exposed to antigen w/o co-stimulatory signal
(a) Mechanism of self tolerance
Which type of hypersensitivity is responsible for acute hemolytic transfusion reaction?
Type II hypersensitivity (cytotoxic) is responsible for ABO incompatibility
-when antigen exposure causes direct cellular destruction by MAC formation and complement degredation or opsonization
Which classes of antibodies provide immunity to the fetus?
IgG crosses the placenta => provides infants w/ passive immunity
IgA is expressed in secretions (saliva, tear,s breast milk) so is responsible for the immunologic benefit of breast feeding
Two structures that drains lymphatics into venous system
Right lymphatic duct drains right side of the body above the diaphragm
Then the thoracic duct drains everything else into the junction of the left subclavian and the internal jugular vein
What occurs in the marginal zone of the spleen btwn the red and white pulp?
Marginal zone contains APCs that present antigens to lymphocytes
X-linked agammaglobulinemia
(a) What is it?
(b) Clinical manifestation- age and symptoms
(c) Serum findings
X-linked agammaglobulinemia
(a) B cell immunodeficiency due to mutation that inhibits B cell mutation
(b) Presents around 6 mo (after passive immunity IgG from mom decreases) w/ recurrent bacterial and enteroviral infections
(c) Absent B cells on peripheral smear, low/no Ig of all classes
- absent/scant lymph nodes
X-linked agammaglobulinemia vs. SCID
Both present in early childhood, basically after 6 mo once maternal IgG passive immunity declines
- X-linked agammaglobulinemia is a B cell d/o => recurrent bacerial and enteroviral infections
- SCID is both B and T cell d/o (b/c w/o T cells you don’t activate B-cells) => recurrent viral, bacterial, fungal, and protoxoa infections.
B-cell deficiencies => bacterial infections vs. T-cell deficiencies => viral and fungal infections
Live attenuated vaccine vs. inactivated vaccine
(a) Injected material
(b) Response induced
(c) Advantage over the other
2 types of vaccines
(a) Live attenuated has lost its pathogenicity but transiently retains capacity to grow in the host, while inactivated is inactivated completely while maintaining epitope on cell surface
(b) Live attenuated induces both cellular and humoral response => strong and often lifelong immunity
(c) Inactivated mainly induces humoral response => weaker response, booster shots often required, but no risk of reverting to virulent form
Cytokine responsible for
(a) Recruiting WBC to site of injury
(b) Vascular leakiness to mediate septic shock
(c) Activate NK cells
(d) Stimulate macrophages
(e) Activate bone marrow stem cell growth and differentiation
Important cytokines
(a) TNF-alpha secreted by macrophages recruits WBCs
(b) TNF-alpha secreted by macrophages causes vascular leakiness and mediates septic shock in response to infection
(c) IL-12 from macrophages activate NK cells (feedback response)
(d) Activated NK cells (by IL-12 from macrophages) secrete interferon-gamma to stimulate macrophages to kill phagocytosed pathogens
(e) IL-3 from T cells supports growth and differentiation of bone marrow stem cells
Genetic mechanism of encoding for innate vs. adaptive immunity
Innate immunity encoded by germline
Adaptive immunity (T and B cells) produced by variation using VDJ recombination during lymphocyte development
Differentiate opportunistic viral infections seen in T cell vs. B cell deficiencies
T-cell deficiency => increased risk of CMV, EBV, JCV, VZV
B-cell deficiency => increased risk of enterovirus (polio, enterovirus, echovirus
Cyclosporine
(a) Mechanism of action
(b) Indication
(c) Toxicity
Cyclosporine = immunosuppressant
(a) Calcineurin inhibitor = inhibits transcription of IL-2 => blocks T-cell activation
(b) Organ transplant rejection ppx, psoriasis, RA
(c) Nephrotoxic
- can’t be used in kidney transplant rejection ppx (use sirolimus instead)
Explain why IL-12 receptor deficiency results in a reduced level of serum IFN-gamma
IL-12 secreted by macrophages to induce differentiation of T cells to Th1 cells, also activated NK cells
Then in turn Th1 cells (once activated) secrete IFN-gamma to stimulate macrophages => w/o IL-12 and Th1 activation there is reduced IFN-gamma release
Which type of hypersensitivity is
(a) rapid
(b) most delayed
(c) suspected in many autoimmune diseases
Hypersensitivity
(a) Type I (anaphylaxis, atopic) is due to IgE preformed antibodies => very rapid response to antigen exposure
(b) Type IV is cell-mediated (no antibodies) so very delayed
(c) Type II and III are suspected in AI d/o (mostly type II except SLE is type III)
Which 2 immunosuppressants are best for kidney transplant rejection ppx
The kidney “sir-vives” w/ “Sir”olimus (Rapamycin)
-also use Daclizumab (IL-2R monoclonal antibody)
-can’t use cyclosporine and tacrolimus b/c they’re nephrotoxic
8 yo boy brought in for easy bruising
- PE; petechiae, purpura, eczematous patches
- Labs: Plts 30k
- Hx multiple courses of pneumonia and otitis media
Dx?
Dx = Wiskott-Aldrich "WATER": -thrombocytopenia -eczema -recurrent infection
X linked recessive mutation in WAS gene => loss of cellular and humoral response
Which antibody class is responsible for
(a) delayed adaptive response
(b) immediate adaptive response
(c) type I hypersensitivity
(d) protecting against gut infections such as Giardia
Antibody class
(a) IgG = delayed adaptive immune respones
(b) IgM = immediate response
(c) IgE = binds to basophils and mast cells for type I hypersensitivity
(d) IgA is produced by Peyers patch to protect against gut infection
Name some positive acute phase reactants
Liver-produced serum proteins whose concentrations significantly rise in response to inflammation as induced by IL-6
- C-reactive protein
- ferritin, hepcidin
- fibrinogen
- serum amyloid A
Which of the following type of hypersensitivty reaction is responsible for the following:
(a) serum sickness
(b) SLE
(c) ABO incompatibility
(d) Tb skin test
(e) Anaphylaxis
(f) Transplant rejection
Hypersensitivies
(a) Serum sickness due to immune complex deposition (type III)
(b) SLE due to type III
(c) ABO incompatibility (causing acute hemolytic transfusion rxn) type II
(d) Tb skin test type IV (delayed, cellular not antibody)
(e) Anaphyalxis type I
(f) Transplant rejection (graft vs. host) due to delayed cellular (type IV)
Describe the function of the following acute phase reactants
(a) C-reactive protein
(b) ferritin, hepcidin
(c) fibrinogen
Acute phase reactants
(a) CRP works as an opsonin- fixed complement and facilitates phagocytosis
(b) Ferritin and hepcidin work to sequester free iron to inhibit microbial iron scavenging
(c) Fibrinogen promotes endothelial repair
Differentiate the functions of IgG and IgM
IgG responsible for the delayed adaptive while IgM is responsible for the immediate response
Both activate complement by the classical pathway
In a child w/ recurrent severe sinus and respiratory tract infections, what complement deficiency do you have a high suspicion for?
C3 deficiency- C3 is where all 3 pathways (classic, alternative, lectin) converge, so deficiency results in increase risk of infection
Which cells contain the following surface proteins
(a) CD28
(b) CD19
(c) CD56
(d) CD34
(e) CD21
Cell surface proteins
(a) CD28 on T cells for costimulatory signal
(b) CD19 on B cells
(c) CD56 specific marker for NK cells
(d) CD34 on hematopoetic stem cells
- so significant when looking for malignancies
Live attenuated vaccine vs. inactivated vaccine
(a) Injected material
(b) Response induced
(c) Advantage over the other
2 types of vaccines
(a) Live attenuated has lost its pathogenicity but transiently retains capacity to grow in the host, while inactivated is inactivated completely while maintaining epitope on cell surface
(b) Live attenuated induces both cellular and humoral response => strong and often lifelong immunity
(c) Inactivated mainly induces humoral response => weaker response, booster shots often required, but no risk of reverting to virulent form
Which live attenuated vaccines can be given to an HIV+ pt
Only live attenuated vaccine you can give to an HIV+ pt is the MMR
Contraindicated: intranasal influenza, varicella, polio, yellow fever
What determines whether or not a vaccine will require a booster?
Certain antigens don’t contain a peptide component (ex: LPS from G- bacteria) => can’t be presented to MHC by T cells => weakly or non-immunogenic (don’t elicit huge immune response)
While antigens that contain a protein component will activate class switching and immunologic memory -producing one time long time vaccines
Name 7 encapsulated bacteria that ppl w/ splenic dysfunction are at an increased risk of getting infected with
Encapsulated bacteria
- Haemophillus influenza B
- streptococcus pneumonia
- neisseria meningitis
- Group B streptococcus
- Klebsiella
- E coli
- salmonella
Name two histologic findings in pts post-splenectomy
- Howel-Jolly bodies = nuclear remnants in RBC
2. Target cells b/c spleen is supposed to remove misshaped RBCs but not around to
Where do B cells undergo isotype switching
In the germinal centers of lymph nodes B cells undergo isotype switching (2/2 signal from T cells) that mature them into plasma cells
Using one word describe/differentiate the 4 types of hypersensitivity reactions
ACID
Type I: Atopy and anaphylaxis (IgE)
Type II: Cytotoxic (IgG and IgM)
Type III: Immune complex (IgG)
Type IV: delayed
Type IV is the only one that doesn’t use antibodies (cell mediated)
What part of the lymph node enlarges when body is responding to a viral infection
Paracortex enlarges- part containing T cells
Give an example of each of the 4 types of hypersensitivity reactions
ACID
Type I: anaphylaxis (bee sting), atopy
Type II: cytotoxic
- ABO incompatibility (acute hemolytic transfusion rxn)
- Goodpastures disease
- Graves, Guillain-Barre, Myasthenia gravis, pernicious anemia
Type III: immune complex deposition
- SLE
- Arhrus = swelling and inflammation following tetanus vaccine
- Serum sickness
Type IV: delayed cellular response
- transplant rejection
- contact dermatitis (poison ivy)
Relate the mechanism of action of immunosuppressant Daclizumab to SCID
Daclizumab = immunosuppressant, monoclonal antibody against IL-2R
SCID = congenital defect in IL-2R
Which 2 immunosuppressants are MC used for autoimmune conditions
Azathioprine (antimetabolite that inhibits lymphocyte proliferation) and glucocorticoids (inhibits cytokine produciton)
Selective IgA deficiency
(a) Caution during transfusion
(b) Clinical manifestation
(c) Serum findings
Selective IgA deficiency = most common primary immunodeficiency
(b) Can have anaphylaxis (type I hypersensitivity) in response to blood products w/ IgA
Differentiate
(a) Autograft
(b) Allograft
(c) Xenograft
(a) Self graft
(b) Allograft = graft from same species
(c) Xenograft = graft from dif species
4 yo boy w/ fever, rigors, and dyspnea following BCG vaccine administration
- CXR w/ pneumonitis
- Blood specimen w/ acid-fast bacili
Dx? (hint: T-cell immunodeficiency)
IL-12 receptor deficiency
- can present after BCG vaccine
- IL-12 activated Th1 cells => reduced cytotoxic T cell activity
- associated w/ disseminated mycobacterial and fungal infections
Name 2 calcineurin inhibitors
Calcineurin inhibitors inhibit IL-2 transcription => blocks T-cell activation
- cyclosporine
- tacrolimus
Distinguish the components of innate vs. adaptive immunity
Innate immunity- neutrophils, macrophages, NK cells, complement
Adaptive immunity- T cells, B cells, antibodies
6 yo p/w recurrent infections, treated w/ gene therapy for deficiency in adenosine deaminase (ADA)
Dx?
ADA deficiency = 2nd MC cause of SCID
MC defect = defective IL-2R gamma chain
DiGeorge Syndrome
(a) Genetics
(b) Immunology presentation
(c) Other clinical features
DiGeorge = (a) microdeletion of 22q11
(c) ‘CATCH-22”
- cardiac abnormalities: ToF, truncus arteriosus, interrupted aortic arch
- abnormal facies
(b) -thymic aplasia => reduced T-cells- recurrent viral/fungal infxns
- cleft palate
- hypocalcemia 2/2 parathyroid agenesis (failure to develop 3rd and 4th pharyngeal pouches)
Common variable immunodeficiency
(a) What is it?
(b) Age of onset
(c) Serum findings
(d) Clinical findings
CVID
(a) Mulitple etiologies for B cell maturation defect
(b) Can be acquired in early adulthood (like 20/30s)
(c) Normal number of B cells but reduced plasma cells and Ig
Which cells contain the following surface proteins
(a) MHC I
(b) MHC II
(c) CD4
(d) CD8
Cell surface proteins
(a) MHC I on all nucleated cell surfaces (so all except RBCs)
(b) MHC II are on APCs- B cells and macrophages
(c) CD4 on Th2 cells (helper T cells and regulatory T cells)
(d) CD8 on Th1 cytotoxic killer T cells
Cytokine key for
(a) Causing fever
(b) Stimulating acute-phase protein production
(c) Recruiting neutrophils
(d) Differentiating T cells into Th1 cells
(e) Differentiating T cells into Th2 cells
(f) Promoting B cell differentiation and class switching
(g) Calming down the inflammatory response
Important cytokines
(a) IL-1 from macrophages is the main one that causes fever
(b) IL-6 from macrophages stimulates production of acute-phase proteins (CRP, ferritin)
(c) IL-8 recruits neutrophils
(d) IL-12 from macrophages induces differentiation of T cells into Th1 cells
(e) IL-4 from Th2 cells induces differentiation of T cells into more Th2 cells
(f) IL-4 from Th2 cells promotes B cell growth and class switching to IgE and IgG
(g) IL-10 is secreted from Th2 cells (and regulatory T cells) to modulate/attenuate the inflammatory response
Which type of transplant rejection is prevented/reversed w/ immunosuppression?
Immunosuppression (cyclosporine, tacrolimus, sirolimus) given to prevent acute (week to months) rejection
- Prevent hyperacute (w/in minutes) rejection by carefully choosing donor
- Can’t prevent chronic (mo to year) rejection
MC primary immunodeficiency
Selective IgA deficiency
- mechanism unknown, but low IgA w/ normal IgG and IgM
- can be asymptomatic or present w/ current airway and GI infections
Differentiate classical and operant conditioning
Classical conditioning (Pavlov’s dog) = involuntary response to signal
Operant conditioning = voluntary response, due to reinforcement and punishments
Differentiate these two ego defenses: displacement vs. projection
Both are immature ego defenses
- displacement = transfer unwanted feelings onto a neutral person (mad at teacher so mad at mom)
- projection = attribute unacceptable internal impulse to an external source (want to sleep w/ someone so you accuse your significant other of cheating)
Differentiate these two defenses: reaction formation vs. sublimation
Reaction formation is an immature defense when you ward off an idea by doing the opposite (want to sleep w/ boys so become a priest)
While sublimation is a mature defense where you replace an unacceptable wish w/ a similar one that doesn’t conflict w/ your values (angry at father so want to be aggressive, channel that into sports)
Age of onset
(a) ADHD
(b) Separation anxiety d/o
(c) Tourettes
Age of onset
(a) ADHD must present before age 12 for dx
(b) Separation anxiety d/o MC btwn 7-9 yoa
(c) Tourettes: motor and vocal tics both must be present and must start before age 18 for dx
Which type of amnesia is more prominent in Korsakoff syndrome
Korsakoff syndrome (B1 deficiency in alcoholics) see more anterograde than retrograde amnesia
-more inability to form new memories
Differentiate delirium from dementia
Delirium- level of consciousness wax and wanes, change in sensorium is reversible
Dementia- memory loss, w/o affecting level of consciouness, often (but not always: hypothyroidism, B12 levels, NPH) irreversible
Differentiate hallucinations from delusions
Hallucinations are perceptions in the absence of actual external stimuli
While delusions are false believes that persist despite facts proving contrary
Differentiate hallucinations from delusions
Hallucinations are perceptions in the absence of actual external stimuli
While delusions are false believes that persist despite facts proving contrary
Differentiate diagnosis requirements of
(a) Schizophrenia
(b) Schizoaffective d/o
(c) Schizophreniform
(d) Brief psychotic d/o
Dx requirements
(a) Schizophrenia = at least 2 positive symptoms for at least 6 months
(b) Schizoaffective d/o = schizophrenia w/ mood d/o, mood d/o only present w/ psychosis, but psychosis can be present w/o mood disruption
(c) Schizophreniform d/o = schizophrenia that lasts btwn 1-6 mo
(d) Brief psychotic episode = schizophrenia features for under 1 mo, usually 2/2 stress
Differentiate diagnosis requirements of mania vs. hypomania
Mania- at least 3 DIG FAST characteristics, lasts for at least 7 days
Hypomania- 4 or more days, features not severe enough to significantly impair functioning, no psychotic features
Diagnosis requirements of bipolar I vs. II
(a) Cyclothymic d/o
BP I = at least one manic episode, doesn’t necessarily have depressive episode
-basically any full manic episode buys you a dx of bipolar I
BP II = hypomanic and depressive episode
-no episode of full mania
(a) Cyclothymic d/o = hypomania and dysthymia for at least 2 yrs
Describe the concept of atypical depression
Not atypical as in less common, it’s actually the most common subtype, but atypical as in not having the features of the classically describe depression
Hyperphagia, hypersomnia, mood reactivity (can transiently be happy to positive events), hypersensitivity to rejection
First line tx for atypical depression
1st line for all depression: CBT and SSRI
MAOIs are specifically very effective vs. atypical depression, but still not first line b/c of their risk profle
Definition of postpartum mood disturbances
Has to have onset w/in 4 weeks of delivery (so 4 mo after delivery doesn’t count snitches)
Features that make grief pathologic
- Lasting more than 6 mo
- meets major depressive criteria (wt loss, suicidality)
- if includes psychotic symptoms like delusions
Features that make grief pathologic
- Lasting more than 6 mo
- meets major depressive criteria (wt loss, suicidality)
- if includes psychotic symptoms like delusions
What makes a panic d/o out of a panic attack?
Just one panic attack (peaking in 10 mins) doesn’t make a d/o, need to also have the attack followed by a resultant change in behavior due to
- worrying about the consequences of the attack
- worrying about having another
So basically person has to be bothered by the attack significantly for over a month, not just have a panic attack
Differentiate GAD and adjustment d/o
Generalized anxiety d/o is w/ no single trigger and lasts over 6 mo
Adjustment d/o lasts under 6 months and is following an identifiable psychosocial stressor
Distinguish PTSD from acute stress d/o
PTSD when symptoms last over a month
Acute stress d/o: 3 days to 1 mo
Differentiate somatic symptom from factitious disorders
In somatic symptom (conversion, hypochondriac) d/o the deception is unconscious, while factitious d/o the pt is conscious they are being deceptive, but they are doing it for primary (internal) gain
Somatic symptom d/o- pt unaware they’re faking symptoms
Factitious d/o (Munchausen)- pt is aware they’re faking symptoms, but aren’t sure why they’re doing it (doing it for internal gain (sick role) not external like malingering)
Differentiate somatic symptom from factitious disorders
In somatic symptom (conversion, hypochondriac) d/o the deception is unconscious, while factitious d/o the pt is conscious they are being deceptive, but they are doing it for primary (internal) gain
Somatic symptom d/o- pt unaware they’re faking symptoms
Factitious d/o (Munchausen)- pt is aware they’re faking symptoms, but aren’t sure why they’re doing it (doing it for internal gain (sick role) not external like malingering)
Briefly differentiate the three cluster of personality d/o and what they have a genetic association with
“Weird, Wild, Worried”
Cluster A: ‘accusatory, aloof, awkward’ odd/eccentric, genetic association w/ schizophrenia
-paranoid, schizoid, schizotypal
Cluster B: ‘bad to the bone’, genetic association w/ mood and substance d/o
-antisocial, borderline, histrionic, narcissistic
Cluster C: ‘cowardly, compulsive, clingy’, genetic association w/ anxiety d/o
-avoidant, obsessive compulsive, dependent
Differentiate schizoid and schizotypal personality d/o
Both cluster A (weird) personality d/o
Schizoid = distant, content w/ social isolation, voluntary social withdrawal
Schizoid plus odd magical thinking = schizotypal, odd beliefs, eccentric appearance
Differentiate OCD from obsessive compulsive personality d/o
OCD- pt is bothered by their obsessions/compulsions
OC personality d/o when the behavior is consistent w/ the pts beliefs and attitudes
Differentiate borderline and histrionic personality d/o
Both bordering and histrionic are cluster B (wild) personality d/o
Borderline = impulsive, self-mutilation, unstable mood and interpersonal relationships
Histrionic = attention seeking, sexually provocative
Differentiate schizoid and avoidant personality d/o
Schizoid (cluster A- weird) is when pt prefers social isolation, voluntary social withdrawal
Avoidant (cluster C- worried) is when the pt is super shy and hypersensitive to rejection so they’re distant, but they desire relationships
Distinguish the 4 ‘schizoids’ on a spectrum
Schizoid, then add odd thinking and get schizotypal, then add even more odd thinking and get schizophrenia, then add mood d/o and get schizoaffective
What is orexin?
(a) Associated d/o
Orexin = neuropeptide that regulates arousal/wakefulness
(a) Destruction of neurons that produce orexin in the lateral hypothalamus = narcolepsy- get cataplexy (sudden loss of muscle tone)
